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Purpose Our study aims to explore the role and mechanism of lncRNA small nucleolar RNA host gene 14 (SNHG14) in brain injury caused by ischemic stroke (IS). Methods Middle cerebral artery occlusion (MCAO) model and oxygen-glucose deprivation (OGD)-induced primary cortical neurons were used to construct in vitro and in vivo models of IS, respectively. Relative SNHG14, miR-181c-5p and Bcl-2-modifying factor (BMF) expression levels were detected by quantitative real-time PCR. MTT assay, EdU staining and flow cytometry were used to measure cell proliferation and apoptosis. The protein levels of apoptosis marker and BMF were determined using western blot analysis. ELISA assay was performed to assess cell inflammatory response and injury. Results SNHG14 was upregulated and miR-181c-5p was downregulated in MCAO model and OGD-induced primary cortical neurons. Silencing of SNHG14 markedly promoted proliferation, restrained apoptosis and inflammatory response in OGD-induced primary cortical neurons to alleviate neurons injury. In terms of mechanism, miR-181c-5p could be sponged by SNHG14, and its inhibitor reversed the inhibition effect of SNHG14 silencing on OGD-induced neurons injury. Also, BMF was a target of miR-181c-5p, and its overexpression could reverse the suppressive effect of miR-181c-5p on OGD-induced neurons injury. Our data uncovered that BMF expression was positively regulated by SNHG14 and negatively regulated by miR-181c-5p. Conclusion Our results indicated that SNHG14 promoted neurons injury through regulating miR-181c-5p/BMF axis, suggesting that SNHG14 might be a potential target to alleviate IS-induced brain injury.

Background: Most patients with spontaneous pneumothorax(SP) are treated with video-assisted thoracoscopic surgery (VATS) . But it fails to achieve an ideal goal of minimal damage and low cost and may be unsuitable for patients with poor underlying lung condition secondary to COPD. An alternative medical procedure with minimal damage is needed. Aims and Objectives: To explore the efficacy and safety of local pleurodesis plus medical glue assisted argon plasma coagulation (APC) via medical thoracoscopy(MT) in SP patients with subpleural bullae. Methods: The SP patients selected were treated with the following steps.①Adhesiolysis.②Ablating the target bullae with APC.③Spraying medical glue locally on the coagulating sites.④Local pleurodesis(thrombin, erythromycin and 50% glucose injection) on the coagulating sites and lung apex.⑤Chest drain was inserted routinely. Results: 4 patients were included. The average duration of general anesthesia was (97±23)minutes. The postoperative hospitalization time was (10±4) days. The cost was $(2736±675). Ten target bullae(1cm～3cm) were found via MT. The air leak of 2 cases stopped immediately after the treatment while the others stopped on postoperative day 1 and 2 respectively. The transient postoperative fever and chest pain were solved by symptomatic treatment. In the 2 patients with postoperative pleural effusion, pleural drainage was performed in addition. No serious complications occurred. The chest HRCT before discharge showed the target bullae disappeared and the lung reexpanded. Conclusions: Local pleurodesis plus medical glue assisted APC via MT was effective and more minimally invasive in the treatment of SP caused by subpleural bullae.