Monaural cardiopulmonary sound separation via complex-valued deep autoencoder and cyclostationarity.

Objective.Cardiopulmonary auscultation is promising to get smart due to the emerging of electronic stethoscopes. Cardiac and lung sounds often appear mixed at both time and frequency domain, hence deteriorating the auscultation quality and the further diagnosis performance. The conventional cardiopulmonary sound separation methods may be challenged by the diversity in cardiac/lung sounds. In this study, the data-driven feature learning advantage of deep autoencoder and the common quasi-cyclostationarity characteristic are exploited for monaural separation.Approach.Different from most of the existing separation methods that only handle the amplitude of short-time Fourier transform (STFT) spectrum, a complex-valued U-net (CUnet) with deep autoencoder structure, is built to fully exploit both the amplitude and phase information. As a common characteristic of cardiopulmonary sounds, quasi-cyclostationarity of cardiac sound is involved in the loss function for training.Main results. In experiments to separate cardiac/lung sounds for heart valve disorder auscultation, the averaged achieved signal distortion ratio (SDR), signal interference ratio (SIR), and signal artifact ratio (SAR) in cardiac sounds are 7.84 dB, 21.72 dB, and 8.06 dB, respectively. The detection accuracy of aortic stenosis can be raised from 92.21% to 97.90%.Significance. The proposed method can promote the cardiopulmonary sound separation performance, and may improve the detection accuracy for cardiopulmonary diseases.

Silent information regulator type-1 mediates amelioration of inflammatory response and oxidative stress in lipopolysaccharide-induced acute respiratory distress syndrome.

Silent information regulator type-1 (SIRT1) is crucial during the development of acute respiratory distress syndrome (ARDS). We aimed to explore whether SIRT1 activation could protect against ARDS. SIRT1 was activated by its agonist SRT1720. ARDS was induced by intraperitoneal injection of 5 mg/kg lipopolysaccharide (LPS). Lung injuries were determined by the lung wet/dry ratio, inflammatory cells in the broncho-alveolar lavage fluid (BALF) and histological analysis. Inflammatory cytokine release was detected by enzyme-linked immunosorbent assay. The accumulation of neutrophils was detected by myeloperoxidase activity. Oxidative stress was evaluated by malondialdehyde, reduced glutathione, superoxide dismutase and catalase activities. The protein expression levels were detected using western blot. SIRT1 activation, either by SRT1720 administration or recombinant SIRT1, expression eliminated high-dose LPS-induced mortality in mice, attenuated lung injury, influenced cytokine release in BALF and decreased oxidative stress in the lung tissues of ARDS mice. Mechanically, SRT1720 administration inhibited p65 phosphorylation in the lung tissues of ARDS mice. SIRT1 ameliorates inflammatory response and oxidative stress in LPS-induced ARDS.

miR-4458 directly targets IGF1R to inhibit cell proliferation and promote apoptosis in hemangioma.

Hemangiomas (HAs) are benign neoplasms of the vasculature. MicroRNA-4458 (miR-4458) has been reported to function as a tumor suppressor in multiple malignancies, but its biological function in HAs remains unknown. In the present study, the potential role of miR-4458 in HA-derived endothelial cells (HDECs) was investigated. Firstly, reverse-transcription-quantitative PCR analysis was used to confirm the expression of miR-4458 in HDECs following transfection with miR-4458 mimics or inhibitor. Subsequently, MTT and EdU assays were performed and subsequently determined that miR-4458 overexpression significantly inhibited proliferation, and knockdown promoted cell proliferation in HDECs. Flow cytometry analysis revealed that miR-4458 overexpression induced cell cycle arrest, whereas knockdown reversed G0/G1 phase arrest and apoptosis. Furthermore, insulin-like growth factor 1 receptor (IGF1R) was identified as a target of miR-4458. IGF1R knockdown enhanced the effects of miR-4458 on cell proliferation, cell cycle G0/G1 phase arrest and apoptosis in HDECs. Taken together, the results revealed that miR-4458 targeting of IGF1R may serve as a novel therapeutic strategy for treating patients with HAs.