ABSTRACT
To analyze the difficulty, distinction and result of the first national public health practice skills competition among college students, it showed the general situation of this competition, and discussed the present situation, problems and countermeasures of skills training for students majoring in preventive medicine. Based on such competition, educators can promote teaching reform and post competency training.
ABSTRACT
Objective@#To explore the potential therapeutic role of miR-489 in silica-induced pulmonary fibrosis mouse models.@*Methods@#A total of 32 C57BL/6 male mice were randomly divided into four groups: saline, silica, silica plus miRNA control and silica plus miR-489 agomir (n=8 in each group) . The mice were instilled with silica particles suspended in saline or sterile saline intratracheally. Subsequently, miR-489 agomir or miRNA control was injected via the tail vein into each mouse at days 28, 35, 42 and 49, the miR-489 levels, histological examination, collagen deposition, fibrotic biomarkers (E-cadherin, α-SMA, Vimentin, Fibronectin) and transforming growth factor-β1 (TGF-β1) protein levels in mouse lung tissues were measured.@*Results@#miR-489 levels in silica plus miR-489 group were significantly increased in lung tissues compared with silica plus miRNA control group (P<0.05) . Histological examination showed attenuated inflammation, less severe fibrotic foci and less destruction of alveolar architecture in the silica plus miR-489 group. Additionally, both the severity and distribution of lung lesions were ameliorated in silica plus miR-489 group compared with the silica plus miRNA control group (P<0.05) . The collagen deposition and hydroxyproline levels in silica plus miR-489 group were significantly decreased compared with the silica plus miRNA control group (P<0.05) . These changes were supported by decreased protein levels of α-SMA, Vimentin, Fibronectin, TGF-β1 along with increased protein levels of E-cadherin in silica plus miR-489 group (P<0.05) .@*Conclusion@#Our data indicate that the upregulation of miR-489 has potential therapeutic role in silica-induced pulmonary fibrosis in vivo, which may be associated with the depression of TGF-β1 release.