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Artigo em Chinês | WPRIM | ID: wpr-872357

RESUMO

Objective:To analyze the budget execution of infrastructure projects in public hospitals, and to analyze the problems existing in the construction process of infrastructure projects.Methods:The budget execution of infrastructure projects in 13 large-scale public hospitals in a province from 2016 to 2019 was investigated, and the problems in budget execution and the reasons for low budget execution rate were analyzed.Results:Seventeen hospital infrastructure projects in 13 hospitals were generally beyond the planned construction period, and the budget execution rate was generally low. The reasons included the problems of project owner units, project construction units and other external problems.Conclusions:Public hospitals should actively improve the management ability of infrastructure construction, strengthen the whole process management of infrastructure projects, so as to ensure the smooth construction of infrastructure projects and improve the efficiency of capital utilization.

2.
Journal of Medical Research ; (12): 111-113, 2015.
Artigo em Chinês | WPRIM | ID: wpr-464206

RESUMO

Objective To establish the PDGF-BB-induced proliferation of rat pulmonary artery smooth muscle cells(PASMCs), and investigate the effects of the AMPK agonist AICAR on the cell cycle of PASMCs, in order to search new drugs for prevention of pulmo-nary vascular remodeling. Methods 20ng/ml PDGF-BB was used to induced the proliferation of PASMCs, and the effect of 0. 5mmol/L AICAR on the proliferation of PASMCs was observed. Western blot was used to detect the total and phosphorylated AMPK. The prolifer-ation of PASMCs was determined by CCK-8. The mRNA expression of cyclinD1, cyclinE and CDK2/4/6 were detected by flow cytometry analysis cell cycle,quantitative real-time PCR. Results Western blot Results indicated AICAR could promote the activation of AMPK. CCK-8 test Results showed that AICAR blocked the proliferation of PASMCs induced by PDGF-BB. Flow cytometry analysis indicated that AICAR arrested the cell cycle in G0/G1 to S phase. RT-PCR Results demonstrated that AICAR inhibited the mRNA expression of cy-clinD1, cyclinE and CDK2/4/6. Conclusion The AMPK agonist AICAR can block the proliferation of PASMCs induced through arrest cell cycle in G0/G1-S phase by regulation the mRNA expression of cyclin D1, cyclinE, CDK2/4/6, and AICAR has a potential applica-tion in preventing pulmonary vascular remodeling.

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