During the transferring period of education in military college, the teacher building was strengthened. A series of systems was established to enhance ability and passion of teaching and insure the teaching quality. The systems included the teaching certification system, the teacher training system and the evaluating system. This paper also discussed the pre-class training of teachers and human resources intercoursing between colleges and military units.

Objective:To evaluate the protective effect of Diclipterachinensis polysaccharide P2B on liver cell line L-02 injury in-duced by carbon tetrachloride ( CCl4 ) . Methods:The human liver L-02 cells were cultured, and the injury model was built by CCl4 . The L-02 cells were divided into the normal control group, the CCl4-damaged group, and the P2B sample groups (0. 125, 0. 250 and 0. 500 mg· ml-1 ). The contents of alanine aminotransferase ( ALT), aspartate aminotransferase ( AST), superoxide dismutase (SOD) and malondialdehyde (MDA) were determined by MTT assay. Results:Compared with the CCl4-damaged group, P2B could improve the activity of L-02 cells, and the activity of AST and ALT in the supernatant was significantly reduced, and the content of SOD in the cells was increased and that of MDA was decreased. Conclusion:P2B can significantly prevent L-02 cells from the damage induced by CCl4 in a dose-dependent manner, and the mechanism may be related with the anti-oxidative activity of P2B.

Objective To observe any effect of low intensity pulsed ultrasound (LIPUS) on the expression of integrin-focal adhesion kinase (FAK)-mitogen-activated protein kinase (MAPK) mechanochemical transduction pathway-related proteins in the chondrocytes of rabbits with knee osteoarthritis (OA).Methods Of the 18 New Zealand white rabbits selected for the study,twelve received knee anterior cruciate ligament transection to model OA.The remaining 6 rabbits served as normal controls.At the 4th week after modeling the rabbits were sacrificed and chondrocytes were isolated and cultured in vitro.All the cultured cells were randomly divided into three groups:a normal control group (NC),an OA model group (OA) and an OA model plus LIPUS group (OA + LIPUS).When the cells had been cultured to the 2nd passage,the NC group and OA group cells had received no treatment.The OA + LIPUS group cells were exposed to 40 mW/cm2 of LIPUS for 20 min,once a day for 6 days.The expression of collagen protein type Ⅱ,aggrecan,MMP-13,integrin β1 p-FAK and p-p38,p-ERK1/2 and p-JNK Mapks were detected by Western blotting.Results Compared with the NC group,the expression of collagen type Ⅱ and aggrecan was significantly lower in the OA and OA + LIPUS groups,with more significantly lower expression of collagen type Ⅱ and aggrecan in the OA group than in the OA + LIPUS group.Compared with the NC group,the expression of MMP-13 was significantly higher in the OA and OA + LIPUS groups,with a significantly larger increase in the OA group.Compared with the NC group,the expression of integrin β1 and p-FAK was also significantly higher in the OA and OA + LIPUS groups,with a significantly larger increase in the OA + LIPUS group.Compared with the NC group,the expression of p-p38,p-ERK1/2 and p-JNK was also significantly higher in the OA group,but compared with the OA group,the expression of those kinases was,on average,significantly lower in the OA + LIPUS group.Conclusions LIPUS can inhibit the degradation of collagen type Ⅱ and aggrecan,and inhibit the expression of MMP-13,p-p38,p-ERK1/2 and p-JNK in OA chondrocytes,at least in vitro.At the same time,LIPUS can increase the expression of integrin β1 and p-FAK.The results show that LIPUS may activate an integrin-FAK-MAPK mechanochemical transduction pathway to induce changes in the extracellular matrix of chondrocytes.

ObjectiveThis study aims to investigate the efficacy and underlying mechanism of Da Chaihutang （DCHT） in treating hepatocellular carcinoma （HCC） in vitro and in vivo. MethodWe employed methyl thiazolyl tetrazolium （MTT） assay and crystal violet staining to observe the proliferation of Hepa1-6 liver cancer cells treated with DCHT at different doses （0， 125， 250， 500， 1 000 mg·L^-1） for different time periods （1， 2， 4， 8 days）. The orthotopic liver cancer model was established by injection of 1×10⁶ Hepa1-6 cells into mouse， and then the model mice were randomly assigned into six groups： blank， model， DCHT （0.21， 0.625， 1.875 g·kg^-1， ig， qd）， and positive control （5-fluorouracil， 25 mg·kg^-1， ip， qod）. After 14 days of administration， the mice were sacrificed， and the liver samples were collected and fixed in 4% paraformaldehyde for hematoxylin-eosin （HE） staining. The Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）， Cytoscape 3.7.2， STRING， and DAVID were used for the searching of the key targets of DCHT in treating HCC， the construction of protein-protein interaction （PPI） network， and the Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment. Quantitative real-time PCR was performed to determine the mRNA level of interleukin-6 （IL-6） in Hepa1-6 cells and liver tissue. Western blotting was employed to measure the protein levels of the proteins involved in the mitogen-activated protein kinase （MAPK） and signal transducers and activators of transcription 3 （STAT3） signaling pathways. ResultDCHT （500， 1 000 mg·L^-1） treatment for 4 and 8 days inhibited the proliferation of Hepa1-6 cells in a dose- and time-dependent manner （P<0.05）. The in vivo assay showed that DCHT （high dose， 1.875 g·kg^-1） treatment for 14 days led to high differentiation and unobvious heterogeneity of HCC cells and small necrotic area compared with the model group. Network pharmacology analysis predicted that the potential targets of DCHT in the treatment of HCC were mainly the inflammation cytokines such as IL-6， interleukin-1β （IL-1β）， and tumor necrosis factor-alpha （TNF-α） in HCC microenvironment. The potential signaling pathways involved in the treatment were mainly associated with HCC growth and differentiation， including MAPK and STAT3 signaling pathways. Compared with the blank group， DCHT （1 000 mg·L^-1） treatment for 1， 2， 4， and 8 days down-regulated the mRNA level of IL-6 in Hepa1-6 cells （P<0.05）. Similar results were observed in the livers of mice treated with DCHT （0.625， 1.875 g·kg^-1）. The in vitro assay demonstrated that DCHT （1 000 mg·L^-1） treatment for 4 and 8 days and DCHT （500， 1 000 mg·L^-1） treatment inhibited the phosphorylation of extracellular signal-regulated kinases 1/2 （ERK1/2）， c-Jun NH₂-terminal kinase/stress-activated protein kinase （JNK）， p38 MAPK， and STAT3 in a dose- and time-dependent manner （P<0.05）. The in vivo assay showed that DCHT （0.625 and 1.875 g·kg^-1） treatment only inhibited the phosphorylation of p38 MAPK and STAT3 （P<0.05）. ConclusionThe present study indicates that DCHT can inhibit liver cancer cell proliferation by regulating p38 MAPK/IL-6/STAT3 signaling pathway.