Long non-coding RNA MALAT1 sponges miR-149 to promote inflammatory responses of LPS-induced acute lung injury by targeting MyD88.

Acute lung injury (ALI) caused by sepsis occurs early and the condition is severe, and is also an important reason for accelerating the death of patients. Increasing evidence has identified long non-coding RNA (lncRNA) metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) as a regulator of ALI. However, the potential mechanism underlying MALAT1 on ALI still needs further identification. To explore the mechanisms of gene regulation expression mediated by MALAT1 through miR-149/MyD88 in lung injury inflammation, we constructed a lung injury inflammatory model using the lipopolysaccharides (LPS)-induced method and quantificated the cytokines and signaling cascade molecules as well as miR-149. The MALAT1, myeloid differentiation factor 88 (MyD88), tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and IL-6 levels were significantly increased, and the nuclear factor-κB (NF-κB) pathway was activated, but the miR-149 level was decreased in the LPS-induced ALI model. miR-149 directly targeted both lncRNA MALAT1 and the MyD88 gene. Knockdown of MALAT1 down-regulated the levels of MyD88, TNF-α, IL-1ß, and IL-6, and inhibited the NF-κB pathway. However, MALAT1 knockdown up-regulated the expression of miR-149. Overexpression of miR-149 down-regulated MyD88, TNF-α, IL-1ß, and IL-6 levels, and inhibited the NF-κB pathway. MALAT1 acts as a pro-inflammatory factor in ALI via the miR-149/MyD88/NF-κB axis and is therefore a potential novel therapeutic target for ALI treatment.

[The diagnostic value of flexible bronchoscopy in tracheobronchopathia osteochondroplastica].

OBJECTIVE: To enhance the knowledge of tracheobronchopathia osteochondroplastica (TO), and to describe the value of flexible bronchoscopic diagnosis and treatment for the disease. METHODS: The clinical data, bronchoscopic findings, histological results and the methods and effect of bronchoscopic treatment in 10 patients with TO admitted to Xiangya Hospital between June 2006 and July 2007 were retrospectively analyzed. RESULTS: There were 8 males and 2 females (mean age 46 +/- 16, range 33-76 years). The bronchoscopic appearance of TO was multiple whitish, hard nodules projecting into the tracheal lumen (mostly from the anterior and less from the lateral walls). The lesions were found most frequently in the trachea and major bronchi, and lobar and segmental bronchi were involved less frequently. Nodules were restricted to the anterolateral walls in 7 cases. The distribution of the lesions was diffuse in 5, confluent in 2 and scattered in 3 cases. Six patients received bronchoscopic management, including radiofrequency treatment for 2 patients and argon ion laser treatment for the other 4. The lesions in the airways were reduced and clinical symptoms improved to some extent after treatment. No severe complications occurred during and after the procedures. CONCLUSIONS: The diagnosis of TO can be easily underdiagnosed or misdiagnosed. Flexible bronchoscopy with histological examination is the main method for the diagnosis of TO. Radiofrequency and argon ion laser treatment are safe and effective.

[Effect of ginsenoside Rh2 on immunocompetence of alveolar macrophages in patients with non-small cell lung cancer].

OBJECTIVE: To explore the effect of ginsenoside Rh2 (G-Rh2) on the excretion of cytotoxin-effecting molecule of alveolar macrophages (AM) in patients with non-small cell lung cancer (NSCLC). METHODS: The concentration of tumor necrosis factor (TNF-alpha) and NO in the bronchoalveolar lavage fluid (BALF) and the cultured supernatants of AM in 35 patients with NSCLC were measured by ELISA and enzyme method,and levels of TNF-alpha and NO in the cultured supernatants of AM after being cultivated with IFN-alpha, G-Rh2, and IFN-alpha+G-Rh2 were measured by the same method. RESULTS: AM in all the non-small cell lung cancer patients produced TNF-alpha and NO. The activity of TNF-alpha and NO was lower in the BALF and in the cultured supernatants of AM of the tumor-bearing lungs than that of the non-tumor-bearing lungs. The concentrations of TNF-alpha and NO in the cultured supernatants of AM cultivated with G-Rh2 were higher than those in the control (P<0.05), but there were no significant differences between the G-Rh2 group and IFN-alpha group (P>0.05). The concentrations of TNF-alpha and NO in the cultured supernatants of AM cultivated with both G-Rh2 and IFNalpha were obviously higher than those stimulated with IFNalpha or G-Rh2 (P<0.01) alone. CONCLUSION: G-Rh2 can enhance the excretion of cytotoxin-effecting molecules of AM in patients with NSCLC. The changes are more distinctive when G-Rh2 and IFNalpha have coordinated action.

[Study on the relationship between the polymorphism of p53 gene intron 7 and non-small cell lung cancer (NSCLC) and p53 mutation in NSCLC tissues].

OBJECTIVE: To investigate the relationship between p53 gene intron 7 polymorphism and non-small cell lung cancer (NSCLC). METHODS: One hundred and five patients with NSCLC and 100 controls were selected with case-control analysis. Polymerase chain reaction (PCR), Apa I restriction enzyme digestion and agarose gel electrophoretic separation were used to identify genotypes of p53 intron 7 in peripheral blood. Then, NSCLC biopsy tissues (n=64) and NSCLC paraffin-embedded tissues (n=40) were selected for mutation analysis. PCR products of p53 exons 5-8 were sequenced on an automated sequencer following the identification of intron 7 genotypes as previously described. RESULTS: In NSCLC patients, the homozygote positive for ApaI site in p53 intron 7 was 23.8%, the homozygote negative was 12.34%, and the heterozygote was 63.8%. Whereas in control group, the homozygote positive, the homozygote negative and the heterozygote were 44.0%, 11.0% and 45.0%, respectively (P<0.01). In the second part, mutation rate of p53 exons 5-8 was 20.0%, 50.0% and 52.9% in samples with ApaI positive, negative and heterozygotes, respectively (P<0.05). CONCLUSION: p53 intron 7 ApaI polymorphism may be associated with human NSCLC.

[Medical thoracoscopy in the diagnosis of complicate pleural effusion].

OBJECTIVE: To evaluate the role of medical thoracoscopy in the diagnosis of the pleural effusion of unknown etiology. METHODS: The results of 36 patients with the pleural disease of unknown etiology diagnosed by medical thoracoscopy were retrospectively analyzed, including the pathologic results and the complications. RESULTS: Among the 36 patients, 35 were determined with positive rate of 97.2%, and no serious complications was found. CONCLUSION: Medical thoracoscopy is an important method of diagnosing complicate pleural effusion, and has high positive rate. It is a simple operation, with no serious complication, and fast recovery.

[Clinical value of tumor supplied group of factor combined with CEA in diagnosing tuberculosis pleural effusion and malignant pleural effusion].

OBJECTIVES: To determine the clinical value of tumor supplied group of factor (TSGF) combined with carcinoembryonic antigen (CEA) in diagnosing tukerculosis pleural effusion and malignant pleurul effusion. METHODS: TSGF and CEA were detected by ELISA in 14 patients with tuberculosis pleural effusion and 28 patients with malignant pleural effusion. RESULTS: The average levels of TSGF and CEA in patients with malignant pleural effusion were higher than those with tuberculosis pleural effusion. The diagnostic sensitivity of TSGF and CEA in the malignant pleural effusion was 67.5% and 57.5%, the specificity was 85.7% and 78.6%, and the agreement rate was 72.2% and 62.9% respectively; while the sensitivity, specificity and agreement rate of TSGF combined with CEA were 93%, 67.4%, and 88.9%. CONCLUSION: The sensitivity and agreement rate of TSGF combined with CEA are higher than those of either of the two methods. TSGF combined with CEA is important in differentiating tuberculosis and malignant pleural effusion.