Sleep apnea syndrome (SAS) is a disorder in which respiratory airflow frequently stops during sleep. Alterations in electroencephalogram (EEG) signal are one of the physiological changes that occur during apnea, and can be used to diagnose and monitor sleep apnea events. Herein, we proposed a method to automatically distinguish sleep apnea events using characteristics of EEG signals in order to categorize obstructive sleep apnea (OSA) events, central sleep apnea (CSA) events and normal breathing events. Through the use of an Infinite Impulse Response Butterworth Band pass filter, we divided the EEG signals of C3-A2 and C4-A1 into five sub-bands. Next, we extracted sample entropy and variance of each sub-band. The neighbor composition analysis (NCA) method was utilized for feature selection, and the results are used as input coefficients for classification using random forest, K-nearest neighbor, and support vector machine classifiers. After a 10-fold cross-validation, we found that the average accuracy rate was 88.99%. Specifically, the accuracy of each category, including OSA, CSA and normal breathing were 80.43%, 84.85%, and 95.24%, respectively. The proposed method has great potential in the automatic classification of patients' respiratory events during clinical examinations, and provides a novel idea for the development of an automatic classification system for sleep apnea and normal events without the need for expert intervention.

Insults to the alveoli usually lead to inefficient gas exchange or even respiratory failure, which is difficult to model in animal studies. Over the past decade, stem cell-derived self-organizing three-dimensional organoids have emerged as a new avenue to recapitulate respiratory diseases in a dish. Alveolar organoids have improved our understanding of the mechanisms underlying tissue homeostasis and pathological alterations in alveoli. From this perspective, we review the state-of-the-art technology on establishing alveolar organoids from endogenous lung epithelial stem/progenitor cells or pluripotent stem cells, as well as the use of alveolar organoids for the study of respiratory diseases, including idiopathic pulmonary fibrosis, tuberculosis infection, and respiratory virus infection. We also discuss challenges that need to be overcome for future application of alveolar organoids in individualized medicine.

Coronavirus disease 2019 (COVID-19) has gained prominence as a global pandemic. Studies have suggested that systemic alterations persist in a considerable proportion of COVID-19 patients after hospital discharge. We used proteomic and metabolomic approaches to analyze plasma samples obtained from 30 healthy subjects and 54 COVID-19 survivors 6 months after discharge from the hospital, including 30 non-severe and 24 severe patients. Through this analysis, we identified 1019 proteins and 1091 metabolites. The differentially expressed proteins and metabolites were then subjected to Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis. Among the patients evaluated, 41% of COVID-19 survivors reported at least one clinical symptom and 26.5% showed lung imaging abnormalities at 6 months after discharge. Plasma proteomics and metabolomics analysis showed that COVID-19 survivors differed from healthy control subjects in terms of the extracellular matrix, immune response, and hemostasis pathways. COVID-19 survivors also exhibited abnormal lipid metabolism, disordered immune response, and changes in pulmonary fibrosis-related proteins. COVID-19 survivors show persistent proteomic and metabolomic abnormalities 6 months after discharge from the hospital. Hence, the recovery period for COVID-19 survivors may be longer.

Background: Hemoptysis is a significant clinical entity with high morbidity and potential mortality. Both medical management (in terms of resuscitation and bronchoscopic interventions) and surgery have severe limitations in these patients population. Bronchial artery embolization (BAE) represents the first-line treatment for hemoptysis. This article discusses clinical analysis, embolization approach, outcomes and complications of BAE for the treatment of hemoptysis. Methods: A retrospective analysis of 344 cases, who underwent bronchial arteriography at Tianjin Haihe Hospital between 2006 and 2013. Several aspects of outcome were analyzed: Demographics, clinical presentation, radiographic studies, results, complications and follow-up of BAE. Results: Three hundred and forty-four consecutive patients underwent bronchial arteriography, 336 of 344 patients (97.7%) performed BAE; there were 1530 coils for 920 arteries embolized; the main responsible sources for bleeding were right bronchial artery (29.7%), left bronchial artery (21.6%), combined right and left bronchial trunk (18.4%), right intercostal arteries (13.3%); 61 patients (17.7%) had recurrent hemoptysis within 1 month after undergoing BAE, 74 patients (21.5%) had recurrent hemoptysis over 1 month after undergoing BAE; The common complications of BAE included subintimal dissection, arterial perforation by a guide wire, fever, chest pain, dyspnea, etc. The follow-up was completed in 248 patients, 28 patients had been dead, 21 patients still bleed, 92 patients had lost to follow-up. Conclusions: The technique of BAE is a relatively safe and effective method for controlling hemoptysis . The complications of BAE are rare. Although the long-term outcome in some patients is not good, BAE may be the only life-saving treatment option in patients who are poor surgical candidates.

(1) Background: Abnormal repair after alveolar epithelial injury drives the progression of idiopathic pulmonary fibrosis (IPF). The maintenance of epithelial integrity is based on the self-renewal and differentiation of alveolar type 2 (AT2) cells, which require sufficient energy. However, the role of glutamine metabolism in the maintenance of the alveolar epithelium remains unclear. In this study, we investigated the role of glutamine metabolism in AT2 cells of patients with IPF and in mice with bleomycin-induced fibrosis. (2) Methods: Single-cell RNA sequencing (scRNA-seq), transcriptome, and metabolomics analyses were conducted to investigate the changes in the glutamine metabolic pathway during pulmonary fibrosis. Metabolic inhibitors were used to stimulate AT2 cells to block glutamine metabolism. Regeneration of AT2 cells was detected using bleomycin-induced mouse lung fibrosis and organoid models. (3) Results: Single-cell analysis showed that the expression levels of catalytic enzymes responsible for glutamine catabolism were downregulated (p < 0.001) in AT2 cells of patients with IPF, suggesting the accumulation of unusable glutamine. Combined analysis of the transcriptome (p < 0.05) and metabolome (p < 0.001) revealed similar changes in glutamine metabolism in bleomycin-induced pulmonary fibrosis in mice. Mechanistically, inhibition of the key enzymes involved in glucose metabolism, glutaminase-1 (GLS1) and glutamic-pyruvate transaminase-2 (GPT2) leads to reduced proliferation (p < 0.01) and differentiation (p < 0.01) of AT2 cells. (4) Conclusions: Glutamine metabolism is required for alveolar epithelial regeneration during lung injury.

Human infections with the H7N9 virus could lead to lung damage and even multiple organ failure, which is closely associated with a high mortality rate. However, the metabolic basis of such systemic alterations remains unknown. This study included hospitalized patients (n = 4) with laboratory-confirmed H7N9 infection, healthy controls (n = 9), and two disease control groups comprising patients with pneumonia (n = 9) and patients with pneumonia who received steroid treatment (n = 10). One H7N9-infected patient underwent lung biopsy for histopathological analysis and expression analysis of genes associated with lung homeostasis. H7N9-induced systemic alterations were investigated using metabolomic analysis of sera collected from the four patients by using ultra-performance liquid chromatography-mass spectrometry. Chest digital radiography and laboratory tests were also conducted. Two of the four patients did not survive the clinical treatments with antiviral medication, steroids, and oxygen therapy. Biopsy revealed disrupted expression of genes associated with lung epithelial integrity. Histopathological analysis demonstrated severe lung inflammation after H7N9 infection. Metabolomic analysis indicated that fatty acid metabolism may be inhibited during H7N9 infection. Serum levels of palmitic acid, erucic acid, and phytal may negatively correlate with the extent of lung inflammation after H7N9 infection. The changes in fatty acid levels may not be due to steroid treatment or pneumonia. Altered structural and secretory properties of the lung epithelium may be associated with the severity of H7N9-infection-induced lung disease. Moreover, fatty acid metabolism level may predict a fatal outcome after H7N9 virus infection.