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OBJECTIVE@#To explore the expression of the RNA-binding protein tristetraprolin in lung adenocarcinoma cells and its molecular mechanism for inhibiting autophagy.@*METHODS@#Quantitative real-time PCR and Western blotting were performed to detect the expression of autophagy-related genes (including Beclin1, LC3-Ⅱ/LC3-Ⅰ and SQSTM1/p62) in cultured lung adenocarcinoma cells at 24, 48 and 72 h after transient transfection with a tristetraprolin-overexpressing plasmid and the empty plasmid. The effects of transfection with the tristetraprolin-overexpressing plasmid and empty plasmids in the presence or absence of tumor necrosis factor- (TNF-) on the expressions of nuclear factor-κB (NF-κB) p65, c-rel, and p50 were examined in lung adenocarcinoma cells using immunofluorescence assay and Western blotting. The cells were also transfected with the IκBα-mut plasmid and the tristetraprolin-overexpressing plasmid, either alone or in combination, and the changes in the expressions of tristetraprolin and autophagy-related genes were detected using RT-qPCR and Western blotting.@*RESULTS@#The expressions of tristetraprolin were significantly reduced at both the mRNA and protein levels in lung adenocarcinoma cells ( < 0.001). Overexpression of tristetraprolin in the cells significantly lowered the expressions of autophagy-related genes Beclin1 and the ratio of LC3-Ⅱ/LC3-Ⅰ at the mRNA and protein levels ( < 0.001), obviously lowered the expressions of NF-κB p65 and c-rel, and almost totally blocked the nuclear translocation of NF-κB p65 and c-rel ( < 0.05); the expression of p50, however, did not undergo significant changes in response to tristetraprolin overexpression ( > 0.05). The inhibitory effect of tristetraprolin overexpression on autophagy was abrogated by transfection of the cells with IκBα-mut plasmid, which blocked the NF-κB signaling pathway. Co-transfection of the cells with IκBα-mut also attenuated the inhibitory effect of tristetraprolin overexpression on Beclin1 and the LC3-Ⅱ/LC3-Ⅰ ratio at both the mRNA and protein levels ( < 0.05).@*CONCLUSIONS@#The expression of tristetraprolin is low in lung adenocarcinoma cells. Tristetraprolin overexpression causes inhibition of autophagy in lung adenocarcinoma cells possibly by blocking NF-κB p65 and c-rel nuclear translocation.
Subject(s)
Humans , Autophagy , Cell Line , Lung Neoplasms , NF-kappa B , Signal Transduction , TristetraprolinABSTRACT
Chongqing Medical University established respiratory system course group and implemented "organ-systems-based curriculum" (OSBC) integration teaching reform.OSBC teaching of respiratory system broke the traditional disciplinary-centred teaching pattern,adopted the disease-centred and clinicaloriented teaching curriculum.The course group carried on the comprehensive reorganization to the curriculum contents and the teaching personnel,compiled integrated teaching materials,optimized teaching methods and evaluation system.OSBC teaching of respiratory system has so far made some achievements,but the integration of different disciplines,the teaching ability of teachers and the students' coordination with OSBC courses still need to be further improved.
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<p><b>BACKGROUND</b>To evaluate the efficacy and toxicity of gemcitabine and carboplatin (GC) versus paclitaxel and carboplatin (TC) in the treatment of non-small cell lung cancer (NSCLC).</p><p><b>METHODS</b>A total of 64 patients with advanced NSCLC diagnosed by pathology were randomly divided into two groups. Gemcitabine and carboplatin were administrated to the patients in GC group (n=30), and paclitaxel and carboplatin in the TC group (n=34), 28 days as a cycle. All patients received at least two cycles.</p><p><b>RESULTS</b>The overall response rate was 53.3% in the GC group and 58.8% in the TC group (P > 0.05). The main toxicities were well tolerated and consisted of leukopenia, nausea, vomiting and peripheral neuritis, which occurred more frequently in the TC group than in the GC group (P < 0.05).</p><p><b>CONCLUSIONS</b>Both of the two regimens of gemcitabine plus carboplatin and paclitaxel plus carboplatin are feasible, well tolerated and effective in the treatment of NSCLC, and the former may be safer than the latter.</p>
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Objective To investigate the risk factors for nosocomial pulmonary fungal infection(PFI) in COPD patients.Methods The data of 44 cases of nosocomial PFI were analyzed from Jan 2000 to Jun 2003 in Department of Pulmonary Medicine,the First Hospital of Chongqing Medical University.44 cases of COPD patients were randomized as control.Results According to univariate analysis ,the risk factors associated with nosocomial pulmonary fungal infection include those of long-term use of broad-spectrum antibiotics,long-term use of adrenocortical steroid,diabetes mellitus,type Ⅱ respiratory failure,mechanical ventilation and hypoalbuminemia.But according to multivariate logistic regression analysis long-term use of broad-spectrum antibiotics,hypoalbuminemia,mechanical ventilation diabetes mellitus were risk factors.Conclusion Long-term use of broad-spectrum antibiotics,hypoalbuminemia,mechanical ventilation and diabetes mellitus are independent risk factors for nosocomial pulmonary fungal infection in COPD patients.
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objective: To evaluate the effect of high agglomerative staphylococoin(HAS) in the treatment of malignant pleural effusion.Methods: Fifty six lung cancer patients with malignant pleural effusion were randomly divided into two groups.Group Ⅰ were treated with HAS,Group Ⅱ were treated with cisplatin.Results: According to the reduction of the volume of effusion,the effective rates in GroupⅠ and Ⅱ were 82.1% and 42.9% respectively.The karnofsky score was increased.Conclusion: Therapy of HAS can effectively control the malignant pleural effusion and improve the life quality of the lung cancer patients.
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Objective:To study the Pathological changes in lungs of rats infected with Pneumocystis carinii pneumonia after treatment with bilodalide(BL). Methods:PCP rat models were established of hypodermic injection of dexamethasone twice a week for 6 weeks. The PCP rats were treated with BL 30mg/(kg.d)?8days and killed to obtain lungs. Pathological changes in lung tissues were observed under light and electron microscope .Infected and normal rats were established as controls. Results: The number of Pc cysts was markedly reduced in the lung print smear and inflammation in the lung was lightened. The investigation of thinner lung tissue section by transmission electronic microscope showed that the Pneumocystis carinii treated with bilobalide had formation of vacuoles in trophozoites,swelling and destroying of cell organ, rupture of cytomembrane and some high density electronic granulae were investigated in the cytoplasm. Membrane of cyst was destroyed too. Conclusion:Bilodalide can kill Pc and alleviate inflammation in the lung tissues of PCP rats.
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Objective:To study the susceptible factors,clinical feature and treatment of nosocomial pulmonary fungal infection in respiratory patients.Methods:The clinical files of 86 patients with nosocomial pulmonary fungal infection admitted from Jan 2001 to Jun 2004 in Department of Pulmonary Medicine,the First Affiliated Hospital of Chongqing Medical University were reviewed.Results:incidence of nosocomial pulmonary fungal infection was 1.7%.COPD was the main predisposing disease,and Candidiasis was the most.The frequent susceptible factors associated with nosocomial pulmonary fungal infection included long-term use of broad-spectrum antibiotics,long-term use of adrenocortical steroid,hypoalbuminemia,mechanical ventilation,and diabetes mellitus.Clinical feature was non-specific.Fluconazole had better clinical effects on treatment.Conclusion:Nosocomial pulmonary fungal infection is an important cause of the secondary infection in respiratory disease.The clinical feature is non-specific.Clinicians should pay close attention to it.