In this study, we explored to detect the effects and mechanism of bonemarrow-derived mesenchymal stem cells (BMSCs) on ventilator-induced lung injury (VILI). We transplanted BMSCs in mice and then induced VILI using mechanical ventilation (MV) treatment. The pathological changes, the content of PaO 2 and PaCO 2 , wet/dry weight ratio (W/D) of the lung, levels of tumor necrosis factor-α and interleukin-6 in bronchoalveolar lavage fluid, and apoptosis were detected. The autophagy-associated factor p62, LC3, and Beclin-1 expression were analyzed by western blot. The quantitative polymerase chain reaction was applied to detect abnormally expressed microRNAs, including miR-155-5p. Subsequently, we overexpressed miR-155-5p in VILI mice to detect the effects of miR-155-5p on MV-induced lung injury. Then, we carried out bioinformatics analysis to verify the BMSCs-regulated miR-155-5p that target messenger RNA. It was observed that BMSCs transplantation mitigated the severity of VILI in mice. BMSCs transplantation reduced lung inflammation, strengthened the arterial oxygen partial pressure, and reduced apoptosis and the W/D of the lung. BMSCs promoted autophagy of pulmonary endothelial cells accompanied by decreased p62 and increased LC3 II/I and Beclin-1. BMSCs increased the levels of miR-155-5p in VILI mice. Overexpression of miR-155-5p alleviated lung injury in VILI mice following reduced apoptosis and increased autophagy. Finally, TAB2 was identified as a downstream target of miR-155-5p and regulated by miR-155-5p. BMSCs may protect lung tissues from MV-induced injury, inhibit lung inflammation, promote autophagy through upregulating of miR-155-5p.

Acute lung injury caused byCandida albicans could result in high mortality and morbidity. MicroRNA-155 (miR-155) and suppressor of cytokine signaling 1 (SOCS1) have been believed to play a key in the regulation of inflammatory response. Whether miR-155/SOCS1 axis could regulate the acute lung injury caused by C. albicans has not been reported. The acute lung injury animal model was established with acute infection of C. albicans. miR-155 inhibitor, miR-155 mimic, and sh-SOCS1 were constructed. The binding site between miR-155 and SOCS1 was identified with dual luciferase reporter assay. Knockdown of miR-155 markedly inhibited the germ tube formation of C. albicans. Knockdown of miR-155 significantly up-regulated the expression of SOCS1, and the binding site between miR-155 and SOCS1 was identified. Knockdown of miR-155 improved the acute lung injury, suppressed inflammatory factors and fungus loading through SOCS1. Knockdown of SOCS1 greatly reversed the influence of miR-155 inhibitor on the cell apoptosis in vitro. The improvement of acute lung injury caused by C. albicans, suppression of inflammatory response and C. albicans infection, and inhibitor of cell apoptosis were achieved by knocking down miR-155 through SOCS1. This research might provide a new thought for the prevention and treatment of acute lung injury caused by C. albicans through targeting miR-155/SOCS1 axis.

Objectives To evaluate the outcomes of bronchial artery embolization (BAE) for the treatment of massive hemoptysis in patients with pulmonary tuberculosis and identify risk factors that influence recurrence. Methods A total of 81 patients with massive hemoptysis who underwent BAE between January 2014 and December 2017 were retrospectively reviewed. All of the patients had either a history of pulmonary tuberculosis or a current diagnosis of pulmonary tuberculosis. Follow‐up ranged from 18 to 66 months. Results Hemoptysis was stopped or markedly decreased, with subsequent clinical improvement in 73 patients, while 11 patients experienced recurrence during the follow‐up period. Systemic‐pulmonary shunts and clinical failure showed a statistically significant correlation with the recurrence rate. The cumulative non‐recurrence rate was 95.3% for 3 months and 81.9% for more than 24 months. Complications were common (12.5%), but self‐limiting. Conclusions BAE is a safe and effective treatment option for the control of massive hemoptysis in pulmonary tuberculosis patients. Systemic‐pulmonary shunts and clinical failure are the risk factors for recurrence.

We constructed a prognostic-related risk prediction for patients with lung adenocarcinoma by integrating multiple omics information of lung adenocarcinoma clinical information group and genome and transcriptome. Blood samples and cancer and paracancerous lung tissue samples were collected from 480 patients with lung adenocarcinoma. DNA and RNA sequencing was performed on DNA samples and RNA samples. The first follow-up was carried out 3 months after discharge. Clinical information of patients including age, gender, smoking history, and TNM stage was collected. The Cox proportional hazard model evaluated more than 600 potential SNPs related to the prognosis of lung adenocarcinoma. After LASSO analysis, we obtained 4 SNPs related to the prognosis of lung adenocarcinoma (including rs1059292, rs995343, rs2013335, and rs8078328). Through the Cox proportional hazard model, 260 candidate genes related to the prognosis of lung adenocarcinoma were evaluated. After subsequent analysis, 3 genes related to the prognosis of lung adenocarcinoma (LDHA, SDHC, and TYMS) were obtained. All survived patients were spilt into a high-risk group ( n = 170 ) and a low-risk group ( n = 170 ) according to 4 SNPs and 3 genes related to the prognosis of lung adenocarcinoma. The overall survival rate of patients in the high-risk group was lower than that in the low-risk group. The prognostic risk prediction index constructed by combining clinical information group and genomic and transcriptome characteristics of multiomics information can effectively distinguish the prognosis of patients with lung adenocarcinoma, which will provide effective support for the precise treatment of patients with lung adenocarcinoma.