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Objective To evaluate the efficacy and safety of high-dose ambroxol in treating acute exacerbations in chronic obstructive pulmonary disease (AECOPD).Methods The trial design was random,open,and parallel control.126 patients with AECOPD were involved.High-dose group received ambroxol 150 mg 3 times per day for 7 days (n=46),while conventional-dose group given ambroxol 30 mg 3 times per day for 7 days (n=40) and control group was given a routine treatment (antibiotic therapy,oxygen inhalation and bronchodilators) (n=40).Results The effective rates of high-dose group and conventional-dose group (95.6 ％,77.5 ％) were significantly higher compared with control group (55.0％) (x2 =19.81,4.53,both P＜0.05).The average duration of hospitalization was significantly lower in high-dose group (10.78 ±0.95)d and conventional-dose group (11.75±0.84)d comparing with control group (13.15±0.89)d (q=11.88,7.24,both P＜0.05).The clinical efficacy in high dose group was much better.Conclusions High-dose ambroxol is a safe and efficient therapy in the treatment of acute exacerbations in chronic obstructive pulmonary disease.
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AIM: To study the possible molecular mechanism of beta-amyloid peptide_ 1-40 -induced apoptosis in rat cortical neurons. METHODS: 40 mg/L beta-amyloid peptide_ 1-40 (A?_ 1-40 ) was used to induce apoptosis in cultured rat cortical neurons. The level of CDK4, phosphorylated pRB were detected by flow cytometry and immunoblotting; RT-PCR was used to examine the mRNA expression of E2F1 while fluorescent spectrofluorometer was used to measure caspase-3 activity. All of the above study was designed to observe whether the level of CDK4, phosphorylated pRB and E2F1 mRNA expression could be affected by A?_ 1-40 . RESULTS: (1)The level of CDK4, phosphorylated pRB increased markedly 2-4 hours after treatment with A?_ 1-40 , and caspase-3 activity elevated remarkably 12-24 hours after treatment with A?_ 1-40 ; (2) E2F1 mRNA expression was upregulated 3 hours after incubation with A?_ 1-40 . CONCLUSION: A?_ 1-40 may induce apoptosis in rat cortical neurons in a manner dependent on CDK4-pRB-E2F1 pathway.