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Based on MOOC teaching mode and the combination of flipped classroom teaching theory,the role of internship practice is integrated into medical education and the combination of MOOC teaching and traditional teaching mode in medical humanities curriculum is explored in practice applications.This paper analyzed the cur-rent situation of medical humanities curriculum teaching operation under current situation; based on the teaching concept of MOOC,introduced the reform of teaching form and teaching method in blending teaching mode,and ex-plored the practical application and practical thinking of blending teaching mode.This mode not only plays a lead-ing role of teachers teaching,but also fully embodies the subjective status of students'learning,exercises the students'ability of thinking in practice at the same time,and is an effective mode to improve medical humanities curriculum teaching.
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At present, many weak points still exist in teaching practices of medical English in medical colleges, such as lack of clear learning goals and prospects for medical English among medi-cal students, as well as the absence of systematic and practical teaching materials, as well as inappro-priate construction of teacher team for teaching practice. Therefore, corresponding modifications on teaching objectives, construction of teacher team and implementation methods for medical English are urgently needed so as to achieve effective teaching and subsequently meet the new international stan-dards for medical education.
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Objective To inVestigate the effect of emodin on hyPertroPhic scar fibroblasts ( HSFs ) and exPlore the underlying mechanism. Methods HSFs were treated by emodin at final concentrations of 0,20,40,and 80 μmol·L-1, resPectiVely,in the cultural media. Forty_eight hours later,the cells were subjected to MTS assay and flow cytometry assay with annexin V and ProPidium iodide as dyeing indicators. Whole cell lysates from the cells of eVery grouP were subjected to Western blotting to measure the Protein exPression leVels of ERK1∕2,Bcl_2,Mcl_1 and RIP1. Results The cell Viability of HSFs was inhibited by emodin in a dose dePendent manner. The mortality rate of HSFs treated with emodin for 48 h at the concentrations of 40 and 80 μmol·L-1 were 28. 6%and 68. 0%,resPectiVely,which was significantly higher than that of the control grouP ( P<0.01).Pretreatmentwith Z_VAD_FMK could Partially reduce the mortality caused by emodin (P<0.05).PhosPhorylation of ERK1∕2 and the exPression of RIP1 and Mcl_1 were inhibited by emodin. Conclusion Down regulation of ERK1∕2,RIP1 and Mcl_1 by emodin may account for the inhibited Proliferation and increased cell death of HSFs.
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Objective To observe the effect of Vascular Endothelial Growth Factor(VEGF) to the expression in hepatoma cells affected by TGF-?1 and hopxia. Methods HepG2 cells were cultured in vitro, and treated with different doses of TGF-?1 and Cobalt chloride hexahydrate(CoCl2), or with TGF-?1 and CoCl2. The change of VEGF protein and mRNA was detected by immunohistochemistry and semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR). Results Immunohistochemistry and RT-PCR showed that the expression of VEGF protein and mRNA were significantly higher in TGF-?1 groups or CoCl2 groups than that of control group(P
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AIM: To investigate the effect of nitric oxid e (NO) and taurin on hemorrhagic shock /reperfusion injury. METHODS: Twenty-four rabbit s were divided randomly into 3 groups ( n= 8): control group and shock group and taurine group. The model of hemorrhagic shock/reperfusion was used. The activities of ni tric oxide synthase (NOS),superoxide dismutase(SOD),lactate dehydrogenase (LDH)and the contents of malondialdehyde(MDA),nitric oxide pvoducts( NO - 2/NO - 3) in plasma were observed before shock and shock 1.5 h,reper fusion 1 h ,2 h and reperfusion 3 h. RESULTS: ①During shock/reperfusion, the ac tivities of NOS,LDH and the contents of MDA,NO - 2/NO - 3 were significan tly highe r, but the activity of SOD was significantly lower in plasma of shock group than that of before shock and shock 1.5 h. ②At 3 h reperfusion, the activity of NOS and the contents of MDA, NO - 2/NO - 3 were significantly higher,bu t the act ivity of SOD was significantly lower in the lung and heart of shock group than t hat of control group. ③ Taurine(40 mg?kg -1 ,iv) attenuated all the c hanges above mentioned at total time points of reperfusion. ④ A close correlation was shown between MDA content and NO - 2/NO - 3 content in plasma, lung and i n heart. CONCLUSION: These results suggeste that NO may be involved in oxida nt-mediated shock/reperfusion, antagonistic effect of taurine on hemorrhagic shock/reperfusi on injury may be relate d to decreasing the generation of NO and anti-lipoperoxidation.
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AIM:To investigate whether Smad pathway participates the process of extracellular signal regulated kinase (ERK) induced the proliferation of vascular smooth muscle cells (VSMCs). METHODS: Human umbilical artery smooth muscle cells (hUASMCs) were divided into four groups: control group, PDGF (platelet derived growth factor) group, ERK blocking agent group and PDGF+ERK blocking agent group. MTT assay was used to detect the proliferation of hUASMCs (A value). Immunohistochemical technique was used to detect the expression of PCNA, phosphorylated ERK (p-ERK) and phosphorylated Smad2/3 (p-Smad2/3) protein in hUASMCs. The expression of Smad2/3 mRNA in hUASMCs was detected by RT-PCR. RESULTS: The proliferation of hUASMCs and the expression of PCNA, p-ERK and p-Smad2/3 proteins in hUASMCs in PDGF group were increased obviously than those in other groups (P