Endovascular treatment for massive haemoptysis due to pulmonary pseudoaneurysm: report of 23 cases.

PURPOSE: To evaluate the safety and effectiveness of endovascular treatment for massive haemoptysis caused by pulmonary pseudoaneurysm (PAP). METHODS: The clinical data, imaging data, and endovascular treatment protocol of 23 patients with massive haemoptysis caused by continuous PAP were retrospectively analysed. The success, complications, postoperative recurrence rate, and influence of the treatment on pulmonary artery pressure were also evaluated. RESULTS: Nineteen patients with a bronchial artery-pulmonary artery (BA-PA) and/or nonbronchial systemic artery-pulmonary artery (NBSA-PA) fistula underwent bronchial artery embolization (BAE) and/or nonbronchial systemic artery embolization (NBSAE) + pulmonary artery embolization (PAE). The pulmonary artery (PA) pressures before and after embolization were 52.11 ± 2.12 (35-69 cmH2O) and 33.58 ± 1.63 (22-44 cmH2O), respectively (P = 0.001). Four patients did not have a BA-PA and/or NBSA-PA fistula. Embolization was performed in two patients with a distal PAP of the pulmonalis lobar arteria. Bare stent-assisted microcoils embolization was performed in the other two patients with a PAP of the main pulmonary lobar arteries. The PA pressures of the four patients before and after treatment were 24.50 ± 1.32 (22-28 cmH2O) and 24.75 ± 1.70 (22-29 cmH2O), respectively (P = 0.850). The technique had a 100% success rate with no serious complications and a postoperative recurrence rate of 30%. CONCLUSION: Endovascular treatment is safe and effective for massive haemoptysis caused by PAP. BAE and/or NBSAE can effectively reduce pulmonary hypertension in patients with a BA-PA and/or NBSA-PA fistula.

The expression of myosin-regulated light chain interacting protein (MYLIP) in lung cancer and its inhibitory effects on lung carcinomas.

BACKGROUND: This study explored the relationship between myosin-regulated light chain interacting protein (MYLIP) and the prognosis of lung cancer and its effects on the proliferation, migration, and invasion of lung cancer cells. METHODS: Bioinformatics analyses of databases were conducted to explore the relationship between the expression of MYLIP and the prognosis of lung cancer patients. Real-time fluorescent quantitative polymerase chain reaction and Western blot analyses were used to measure the levels of MYLIP expression. Cell counting kit-8 (CCK8) and cell cloning experiments were used to determine the effects of MYLIP on cell proliferation. The scratch test and invasion experiments were conducted to assess the effects of MYLIP on the migration and invasion of lung cancer cells. Tumor formation experiments were performed in nude mice to determine the effects of MYLIP on tumor growth. RESULTS: The mRNA and protein expression of MYLIP in cancer tissues from lung cancer patients were significantly lower than that found in normal adjacent tissues (P<0.05). Bioinformatics analysis showed that lung cancer patients with high MYLIP expression had a better prognosis compared to patients with low MYLIP expression. The results of the CCK8 and cell proliferation experiments revealed that the proliferation ability of lung cancer cells overexpressing MYLIP was significantly lower than that of control cells (P<0.05). The scratch experiment and invasion experiments demonstrated that the scratch closure rate and the cell invasion ability of lung cancer cells overexpressing Experiments in nude mice showed that the tumor-forming ability of lung cancer cells with high expression of MYLIP was weaker than that of the control group, and the tumor growth rate and the tumor weight were also lower than that of the control group (P<0.05). CONCLUSIONS: Low levels of MYLIP expression were detected in the cancer tissues of lung cancer patients, and its expression levels were positively correlated with the prognosis of lung cancer. Furthermore, MYLIP had a significant inhibitory effect on the proliferation, migration, and invasion of lung cancer cells, suggesting that MYLIP may be a tumor suppressor gene for lung cancer. The results may have significant potential for clinical applications.