Abstract.A 53-year-old male was admitted to Xinhua Hospital (Shanghai, China) due to coughing and dyspnea that had persisted for half a year, with aggravation of chest tightness and dyspnea for 1 week. Chest computed tomography (CT) revealed a mass within the distal third of the trachea. Flexible bronchoscopy confirmed an ~2.0 cm, smooth, tan-colored mass in the trachea, 2 cm above the carina. Endoscopic resection by argon plasma coagulation combined with electronic snaring was applied, however, recurrence was found 2 weeks later. Finally, the tumor was completely removed by surgery and the post-operative course was uneventful. Since schwannoma is rare in the intrapulmonary region and extremely rare in the trachea, a review of 51 cases of primary tracheal schwannoma previously reported in the English literature was performed. The majority of cases occurred in adults and were usually located in the distal third of the trachea. The predominant tumor size was 1-3 cm and airway obstruction symptoms were common. Half of the patients were misdiagnosed with asthma, and CT scan and bronchoscopy were contributory to the correct diagnosis. The treatment of choice depended on the patient's condition, however, surgery should be chosen in the event of local recurrence following endoscopic treatment.

Background: Increasing evidences have underlined the importance of long non-coding RNAs (lncRNAs) in human malignancies. LINC00958 has been found involved in some cancers. However, the underlying mechanical performance of LINC00958 in lung adenocarcinoma (LAD) has not been explored yet. Methods: The expression of relevant mRNA and protein were measured by qRT-PCR and western blot assays. EdU, colony formation, TUNEL and transwell assays were performed to investigate the function of LINC00958 on LAD progression. Luciferase reporter, RNA pull down and RIP assays were conducted to investigate the molecular mechanism of relevant RNAs. Results: LINC00958 was found notably overexpressed in LAD, which was associated with the stimulation of its promoter activity induced by SP1. LINC00958 depletion dramatically inhibited LAD cell proliferation, migration and invasion capacities by acting as a miR-625-5p sponge. MiR-625-5p curbed LAD progression via targeting CPSF7 and down-regulating its expression. Mechanically, LINC00958 was identified as a competing endogenous RNA (ceRNA) and positively regulated the expression of CPSF7 via sponging miR-625-5p. Conclusions: LINC00958 might drive LAD progression via mediating miR-625-5p/CPSF7 axis, indicating the potential of targeting LINC00958 for the treatment of LAD.

Four distinct clinical phenotypes of asthma were identified by cluster analysis. The results of the MSCT and pathological examinations may suggest specific pathogeneses among the phenotypes.

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