OBJECTIVE:To study the in vivo antibacterial effects of Norfloxacin injection in animals.METHODS:After infecting the animals by injection of Escherichia coli and Staphylococcus aureus suspension into the mice's abdominal cavity and rabbit's body,the animals were divided into therapy,prophylaxis and control groups to observe the effect of Norfloxacin.RESU-LTS:All mice of control group died within 24 hours after the injection of bacteria while those of the therapy and prophylaxis groups survived.The results of experiment on rabbits were similar to those on mice.CONCLUSION:The results show that Norfloxacin injection has obvious therapeutic and prophylactic effects on infections induced by E.coli and Staphylococcus aureus.

Objective To study the mechanics of moderate and severe brain injury of pedestrians in road traffic accident by establishing the virtual model of impact occipital bone injury.Methods The clinical data were used to analyze comlnon mode and characteristics of moderate and severe brain injury of pedestrians.Then,the corresponding finite element model built by using Hypermesh software was used to to analyze the changes of intracranial pressures and compare with injury characteristics by using Ls-Dyna soft-ware. Results The conlmon injury mode of moderate and severe brain injury of pedestrians wag the con-tact impact of occiputal part,characterized by"eontrecoup injury",mainly including subdural hemorrhage,extradural hemorrhage and contusion in the opposite parts to the impact point.The simtdation resuhs showed that when the impact was at right occiputal bone.the peak value of condensing force decreased from the right occipital lobe.to the left frontal lobe,while the peak value of tension increased gradually and reached maximum at the surface of left frontal lobe. Conclusions Moderate and severe brain injury of pedestrian is commonly caused by impacting the occiputal bone in road traffic accident.The tension deformation in frontal or temporal lobes and the distribution of vessels in grey matter may be main biomeehanies leading to "contrecoup injury".

Objective:To investigate the effect and mechanism of lactoferrin (LF) on biological behaviors of brain glioma cells.Methods:The effect of LF at different concentrations (0, 100, 200 and 300 μg/mL) on the proliferative ability of human glioma cell line U87MG was analyzed by MTT assay to screen the optimal drug concentration. U87MG cells were divided into blank control group and LF (200 μg/mL) treatment group. Edu staining, Transwell assay, Mito-Tracker staining and DCFH-DA staining were used to detect the cell proliferation, migration, mitochondrial activity and reactive oxygen level. Autophagy marker protein microtubule associated protein 1 light chain 3B (LC3B) expression was detected by immunofluorescent chemical staining; contents of superoxide dismutase (SOD) and malonaldehyde (MDA) were detected by colorimetric chemical sensors; expressions of genes related to epithel-to-mesenchymal transformation (E-cadherin, fibronectin, N-cadherin, vimentin and Snail) were detected by reverse transcription (RT)-PCR; expressions of apoptosis-related proteins (Bax and Bcl-2) were detected by Western blotting.Results:Compared with blank control group, the LF treatment group had significantly decreased proportions of Edu positive cells and Mito-Tracker positive cells, number of cell migration and SOD content, and statistically increased proportion of DCFH-DA positive cells, MDA content and LC3B immunofluorescent staining intensity in cytoplasm ( P<0.05). Compared with blank control group, the LF treatment group had significantly decreased E-cadherin mRNA expression and Bcl-2 protein expression, and statistically increased fibronectin, N-cadherin, vimentin and Snail mRNA expressions and Bax protein expression ( P<0.05). Conclusion:LF can effectively inhibit the proliferation, migration, invasion and other biological behaviors of glioma cells, whose mechanism is closely related to mitochondrial activity.

BACKGROUND: MicroRNA-20a (miR-20a) is dysregulated in many types of malignancies, including human hepatocellular carcinoma (HCC), but its expression level and functional significance in HCC are still disputed. We aimed to study the role of miR-20a-5p in HCC and its downstream molecular mechanisms. METHODS: We used real-time polymerase chain reaction to detect the expression of miR-20a-5p and runt-related transcription factor 3 ( RUNX3 ) in HCC and paraneoplastic tissue, transfected Huh7 and highly metastatic human hepatocellular carcinoma (MHCC97H) cells. A live cell workstation was used to observe the proliferation and migration of transfected cells. The invasiveness of transfected cells was verified by Transwell assay. Cell apoptosis was detected by flow cytometry. The expression levels of proteins after transfection were measured using simple western immunoblot measurements. Gene expression profiles between HCC and normal samples were obtained from The Cancer Genome Atlas. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment results were processed by the database for annotation, visualization and integrated discovery. Potential target genes of miR-20a-5p were predicted to further investigate how miR-20a-5p regulates epithelial-mesenchymal transition (EMT) in HCC. RESULTS: MiR-20a-5p was significantly highly expressed in HCC tissues, and overexpression of miR-20a-5p significantly promoted HCC cell proliferation, migration, and invasion and inhibited apoptosis in vitro. The protein expression of E-cadherin was decreased and that of vimentin was increased after overexpression of miR-20a-5p in HCC cells. We discovered the intersection of genes from miRDB, miR TarBase, and TargetScan, obtained 397 target genes and finally focused on RUNX3. RUNX3 was not only reduced in HCC specimens but also drastically reduced in HCC cells overexpressing miR-20a-5p. RUNX3 expression decreased with elevated miR-20a-5p, which activated downstream EMT signaling and promoted cell proliferation, migration, and invasion. CONCLUSIONS Since RUNX3 is involved in EMT in HCC, as proven by previous research, our findings provide further evidence for a novel regulatory pathway comprising the miR-20a/RUNX3/EMT axis that upregulates EMT signaling and enhances the migration of HCC cells.
Humans ; Carcinoma, Hepatocellular/pathology* ; Epithelial-Mesenchymal Transition/genetics* ; Liver Neoplasms/pathology* ; Gene Expression Regulation, Neoplastic/genetics* ; MicroRNAs/metabolism* ; Cell Movement/genetics* ; Cell Line, Tumor ; Cell Proliferation/genetics* ; Core Binding Factor Alpha 3 Subunit/metabolism*