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AIM: To investigate the role of autophagy in the apoptosis of human pulmonary artery endothelial cells (HPAECs) induced by cigarette smoke extract (CSE).METHODS: HPAECs were cultured routinely.HPAECs were treated with CSE at different concentrations, and the cell viability was detected by MTT assay.HPAECs were divided into control group, CSE group, 3-methyladenine (3-MA) group and 3-MA+CSE group.The autophagy was observed under fluorescence microscope with monodansylcadaverine (MDC) staining.Annexin V/propidium iodide staining and Hoechst 33342 staining were employed to detect apoptosis.In addition, the protein levels of LC3, beclin-1 and cleaved caspase-3 were determined by Western blot.RESULTS: MDC staining showed the increased production of autophagic vacuoles was observed in CSE group.The results of Western blot showed that the expression levels of autophagy-related proteins LC3 and beclin-1 were increased, while 3-MA pretreatment inhibited the expression of these proteins and the production of autophagic vacuoles.Observation with Annexin V/propidium iodide staining and Hoechst 33342 staining showed that the apoptotic rate in CSE group was significantly higher than that in control group, and pretreatment with 3-MA induced further increase in the cell apoptosis.The protein level of cleaved caspase-3 in CSE group was significantly higher than that in control group (P<0.05), and 3-MA+CSE treatment induced the further increase in the protein level of cleaved caspase-3.CONCLUSION: CSE induces autophagy and apoptosis in the HPAECs.Inhibition of autophagy promotes the apoptosis induced by CSE in HPAECs, which can be achieved through activation of caspase-3.
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Objective To establish an optimal animal model of pulmonary metastasis of human lung adenocarcino-ma, to serve further investigation of mechanism of lung adenocarcinoma metastasis.Methods Eleven nude mice aged 4-6 weeks were used in this study.Suspension of human lung adnocarcinoma A549 cells (0.1 mL, 107 cells/mL) was injec-ted into the tail vein in nude mice.From four weeks after inoculation, two nude mice were killed each time at 4, 5, 6 weeks after the tumor cell injection at random for examination.The remaining 3 mice were killed at the end of the experi-ment.At autopsy, the lung, brain, liver, kidney and other organs were removed, fixed in neutral buffered formalin and embedded in paraffin.Sections were cut and stained with hematoxylin-eosin, and examined by histopathology.The number of metastatic foci was counted.Results No mouse died after tumor cell inoculation.Serially euthanized mice revealed evi-dence of gradually increasing pulmonary metastases in the mice:No metastasis was found before 4 weeks after tumor cell in-oculation, the first histological metastases appeared at 5 weeks, gross metastatic foci were observed at 6 weeks, widely spread metastatic foci were observed at 7 weeks, and the remain 3 mice developed cachesia at 11, 13, and 14 weeks after tumor cell inoculation.Mediastinal lymph node metastases were found in the nude mice by 11 weeks after tumor cell inocu-lation.Conclusions We have successfully established a nude mouse model of pulmonary metastasis by injecting human lung adenocarcinoma A549 cells into the tail vein.
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OBJECTIVE To investigate the clinical pathologic features and therapeutic tools of pulmonary cryptococcosis.METHODS The clinical data about 16 cases of pulmonary cryptococcosis which were diagnosed by histopathologic examinations were reviewed.The survey data recorded over a 15-year period,from 1982 to 2007,were summarized.We analyzed their clinical situations,radiographic manifestations,final diagnosis and therapeutic tools.RESULTS The majority of the patients were middle-aged males.The health condition of the most of the patients was good before infection.six months to five years after surgery and antifungal theragy,no relapse,dissemination and death were observed.CONCLUSIONS The majority of primary pulmonary cryptococcosis patients have not underlying diseases,and their radiography manifestations show single or multiple nodular shadows,tumor shadows and infiltrative shadows.The limited pathological change can be excised and applied with the antifungal drugs.Fluconazole is the first-choice drug for curing pulmonary cryptococcosis.
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Objective To explore the clinical features and the cause of secondary phosgene poisoning after rescuing the patients with acute phosgene poisoning.Methods According to the diagnostic criteria of occupational acute phosgene poisoning,the differences of clinical manifestation,laboratory results and chest X-ray between secondary poisoning patients and primary patients were compared.Results Among the 25 patients with secondary phosgene poisoning,14(56.0%) had cough,13(52.0%)had throat stimulus,10(40.0%)had chest stuffiness,2(8.0%)had polypnea,1(4.0%) had pain in the eye.There was no significant difference in clinical manifestation between the secondary and primary patients. No positive sign was found after the examination of pulmonary function in the 25 patients,but all of them had abnormal chest X-ray,and typical bronchitis could be found.According to the diagnostic criteria,the 25 patients had slight acute phosgene poisoning,and recovered after treatment for 7 to 10 days.Conclusion To prevent the secondary phosgene poisoning after treating the patients with acute phosgene intoxication,medical workers should enhance protection awareness and take some necessary measures.