Background: The 2019 novel coronavirus (COVID-19) has continuous outbreaks around the world. Lung is the main organ that be involved. There is a lack of clinical data on the respiratory sounds of COVID-19 infected pneumonia, which includes invaluable information concerning physiology and pathology. The medical resources are insufficient, which are now mainly supplied for the severe patients. The development of a convenient and effective screening method for mild or asymptomatic suspicious patients is highly demanded. Methods: This is a retrospective case series study. 10 patients with positive results of nucleic acid were enrolled in this study. Lung auscultation was performed by the same physician on admission using a hand-held portable electronic stethoscope delivered in real time via Bluetooth. The recorded audio was exported, and was analyzed by six physicians. Each physician individually described the abnormal breathing sounds that he heard. The results were analyzed in combination with clinical data. Signal analysis was used to quantitatively describe the most common abnormal respiratory sounds. Results: All patients were found abnormal breath sounds at least by 3 physicians, and one patient by all physicians. Cackles, asymmetrical vocal resonance and indistinguishable murmurs are the most common abnormal breath sounds. One asymptomatic patient was found vocal resonance, and the result was correspondence with radiographic computed tomography. Signal analysis verified the credibility of the above abnormal breath sounds. Conclusions: This study describes respiratory sounds of patients with COVID-19, which fills up for the lack of clinical data and provides a simple screening method for suspected patients.

To explore the effects of chronic intermittent hypoxia (CIH), which mimics sleep apnea syndrome, on the cardiac renin angiotensin system (RAS), and to investigate the cardiac protection of an angiotensin receptor blocker (ARB)telmisartan (TERT) against CIH. 32 healthy male C57B6J mice were randomly divided into CIH, ARB, blank and air control groups. CIH lasted for 12 weeks. Cardiac angiotensin converting enzyme (ACE), angiotensin converting enzyme 2 (ACE 2) and angiotensin II (Ang II) were evaluated by immunohistochemistry. Myocardial apoptosis were assessed by TUNEL assay and myocardial cell ultrastructure were observed under transmission electron microscope. Cardiac ACE expression was higher in the CIH group than in blank and air control groups, which was decreased with TERT treatment. TERT treatment elevated the expression of cardiac ACE 2 and Ang II compared with CIH group. Myocardial cell and capillary endothelial cell apoptosis, mitochondrial injury were most severe in CIH groups, which were mitigated with TERT treatment. CIH changes the expression of cardiac ACE, ACE2 and Ang II, which may cause myocardial damage. TERT protects mice from CIH-linked cardiac damage via modulating the activity of RAS in the hearts.

This study aimed to investigate the potential compensatory role of plasma exosomal microRNAs (miRNAs), particularly miR-320b, in mitigating early myocardial damage in severe obstructive sleep apnea (OSA) patients without comorbidities. AC16 human cardiomyocytes were co-incubated with plasma exosomes isolated from healthy volunteers (Ctrl-exo) and patients with uncomplicated severe OSA (OSA-exo). Functional assays revealed that OSA-exo significantly enhanced AC16 cell viability, promoted proliferation, and reduced apoptosis. RNA sequencing (RNA-seq) identified 14 myocardial function-related mRNAs in AC16 cardiomyocytes differentially influenced by OSA-exo. Out of the 14 mRNAs, FOXM1, a critical regulator of cardiomyocyte stress response, survival, and regeneration, was verified to be upregulated by OSA-exo by RT-qPCR. Bioinformatic analysis predicted a regulatory relationship between miR-320b and FOXM1, which was confirmed by a dual-luciferase reporter assay. MiR-320b was found to be downregulated in OSA-exo by RT-qPCR. MiR-320b overexpression downregulated FOXM1, induced G0/G1 cell cycle arrest, reduced cell viability, and increased apoptosis. In a mouse model of chronic intermittent hypoxia (CIH), myocardial FOXM1 exhibited a biphasic expression pattern during disease progression. After 4 weeks of CIH exposure, the mouse myocardium exhibited significantly increased FOXM1 expression and reduced levels of apoptosis compared to control, suggesting an early compensatory response. However, after 12 weeks of CIH exposure, decreased myocardial FOXM1 expression and increased apoptosis were detected, suggesting that the early compensatory protective mechanism was overwhelmed by myocardial injury caused by chronic hypoxia, leading to enhanced cardiomyocyte apoptosis and consequent FOXM1 downregulation. These results suggested that miR-320b downregulation in OSA-exo may serve as a compensatory mechanism to protect against early myocardial injury through the upregulation of FOXM1, highlighting miR-320b and FOXM1 as potential therapeutic targets for OSA-associated cardiomyopathy.