Treatment of secondary benign airway stenosis after tracheotomy with Montgomery T-tube.

Objective: With the improvement of surgical operation, increasing incidence of secondary benign airway stenosis, as a complication of long-term tracheal intubation and tracheotomy, leads to significant increases in morbidity and mortality. Previous treatment of secondary benign airway stenosis was mainly based on surgical resection and reconstruction. There is an urgent need for new treatment methods except surgery, especially for those inoperable patients. Methods: This study retrospectively reviewed 20 patients who had treatments of secondary benign airway stenosis after tracheotomy with Montgomery T-tube. The clinical data including clinical features, efficacy, complications and prognosis were retrospectively evaluated. Results: Complete airway obstruction was 12/20, partial stenosis was 8/20, combined with airway granuloma and endoscopic granulation resection was 16/20, combined with scar stenosis and endoscopic balloon dilatation was 18/20. Plugging successfully was 19/20. Complications included mucous accumulation (20/20), secondary granulation tissue formation (13/20), subcutaneous soft tissue infection (1/20), and T-tube re-implantation (3/20). Conclusions: Montgomery T-tube implantation under rigid bronchoscopy is a safe, feasible and effective tracheal forming method with well tolerance for patients with benign airway stenosis. Secondary benign airway stenosis after tracheal intubation and tracheotomy is an indication of Montgomery T-tube implantation. Compared with the traditional tracheotomy, the advantage of Montgomery T-tube implantation is easy to make the patient phonate, significantly improving the quality of life of patients. T-tube implantation is safe, and the postoperative complications include mucous accumulation and formation of secondary T-tube granulation tissue.

Long non-coding RNA DGCR5 is involved in the regulation of proliferation, migration and invasion of lung cancer by targeting miR-1180.

Accumulating studies have demonstrated that non-coding RNAs (ncRNAs), including small non-coding RNAs (small ncRNAs) and long non-coding RNAs (lncRNAs), are involved in tumor growth in lung cancer (LC). However, the specific role of DGCR5 in LC progression is not yet clear. In the present study, we found that DGCR5 was downregulated and miR-1180 was upregulated in the sera and tissues of LC patients and was correlated with poor prognosis. We also found that DGCR5 suppressed proliferation, migration and invasion of LC cell lines H520 and H1299. In addition, a luciferase reporter gene assay was used to investigate the regulatory relationship between DGCR5 and miR-1180. Furthermore, we suggested that DGCR5 inhibited the expression of AKT, GSK-3ß, and ß-catenin by targeting miR-1180. Based on these findings, DGCR5 might serve as a potential target for the development of effective anti-neoplastic therapies in lung cancer.

Cold snare resection for the treatment of benign airway lesions.

The objective was to assess the safety and outcome of cold snare technique used by flexible bronchoscopy in the treatment of airway benign neoplasms. The clinical data of 21 patients, who had airway benign neoplasm and were treated through the cold snare method in Sir Run Run Shaw Hospital, affiliated with the Zhejiang University, were retrospectively analyzed. The relief of the symptoms and occurrence of complications were observed and evaluated. All the tumors were benign and removed by cold snare. Postoperatively, we found that the treatment was completely effective in 12 patients, and there was a significant improvement in 7 patients and a moderate improvement in 2 patients, and no recurrence in follow-up visit. In conclusion, the cold snare technique is an economically feasible, safe, and effective method in the treatment of airway neoplasms.

Effects of SASH1 on lung cancer cell proliferation, apoptosis, and invasion in vitro.

The purposes of this study were to investigate the effects of the SASH1 gene on the growth, proliferation, apoptosis, invasiveness, and metastatic potential of lung cancer cells and explore the potential use of SASH1 for the treatment of human lung cancer. The SASH1 gene was cloned into the pcDNA3.1 eukaryotic expression vector, and SASH1 shRNA were designed and constructed. The resulting constructs were transfected into A549 human lung cancer cells, and the changes in the relevant biological characteristics of the cells overexpressing SASH1 and cells with downregulated expression of SASH1 were analyzed using the MTT assay, transwell invasion assay, and flow cytometry. The effects of the SASH1 gene on the expression of cyclin D1, Bcl-2, and MMP-2/9 were also concurrently examined. In the A549 cells from the pcDNA3.1-SASH1 transfected group, cell viability, proliferation, and migration were significantly reduced compared to the control cells (p = 0.039, p = 0.013), and a cell cycle arrest in G1 was observed. The A549 cells transfected with the SASH1 shRNA demonstrated significantly higher cell viabilities, proliferation, and migration compared to the control cells (p = 0.012, p = 0.045). Additionally, the percentage of A549 cells undergoing apoptosis was significantly higher in the pcDNA3.1-SASH1 transfected cells and significantly lower in the SASH1 shRNA transfected cells compared to the control cells (p = 0.010, p = 0.000). The cyclin D1, Bcl-2, and MMP-9/2 protein expression levels were significantly lower in the pcDNA3.1-SASH1-transfected cells and were significantly higher in the SASH1 shRNA-transfected cells than that in the control cells. The SASH1 gene may inhibit A549 cell growth and proliferation as well as promote cellular apoptosis. The overexpression of the SASH1 gene may also be related to the decreased migration of A549 human lung cancer cells.