AIM: To examine the effect of pretreatment with low-concentration of 11, 12-epoxyeicosatrienoic acid(EET) on myocardial ischemia/reperfusion injury in rats. METHODS: After tracheotomy, myocardial ischemia/reperfusion was produced by occlusion and release of the left anterior descending artery(LAD) of the rats. Ischemic preconditioning(IP) was made by two times of ischemia (5 min)/reperfusion (5 min). The experiment was conducted in three groups: control,IP and pretreatment with 11,12-EET(6.24?10 -8 mol/L), and each group was subdivided into two subgroups:A,the rats were subjected to ischemia (10 min)/reperfusion (10 min) and arrhythmias during the whole periods were monitored; The rats in B were subjected to ischemia (60 min)/reperfusion (30 min) and arrhythmias, cardiac funtion and myocardial infarction size were documented. RESULTS: Both IP and pretreatment with 11,12-EET could protect the heart against arrhythmias, cardiac disfunction and myocardial infarction. CONCLUSION: Pretreatment with 11,12-EET had protective effect on myocardium in case of ischemia/reperfusion, which was similar to ischemic preconditioning.

Objective To explore the influence of chronic neuropathic pain on cellular immune function of mice models.Methods The mice models were established by ligating tibeal nerve and common peroneal nerve on one side,and the influence of chronic neuropathic pain on cellular immune function and tumor necrosis factor-?(TNF-?) and interleukin-6(IL-6) was observed with lymphocyte cell increase experiment(MTT method) and enzyme linked immunosorbent assay(ELISA).Results The increased reactivity of T lymphocyte of the model group was significantly higher than that of the sham group and the control group.At the same time,content of TNF-? and IL-6 in blood of the model group also increased.Conclusion Cellular immune function of mice is increased in the state of chronic neuropathic pain.

AIM: In order to study the relationship between the ERK and p38 MAPK activation and the protection of 11, 12-epoxyeicosatrienoic acid (11, 12-EET) and ischemia preconditioning (IP), the effects of 11, 12-EET and ischemic preconditioning on phosphorylated ERK and p38 MAPK during ischemia and reperfusion in rat myocardium were examined. METHODS: The rat heart was subjected to ischemia for 5 min by ligating the left anterior descending coronary artery followed by reperfusion for 5 min (two times) to undergo ischemia preconditioning. The rats were divided into 5 groups: (1) control; (2) sham group; (3) ischemia/reperfusion (I/R) group, in which the rat heart suffered from 60 min ischemia followed by 30 min reperfusion; (4) IP plus I/R group; (5) EET plus I/R group, in which 6.28?10 -8 mol/L 11, 12-EET was injected intravenously 20 min before I/R. The heart function was examined, and phosphorylated ERK and p38 MAPK were detected by Western blot. RESULTS: At 30 min reperfusion, +dp/dt max ,-dp/dt max and LVDP decreased significantly in I/R group compared with sham group, IP plus I/R group and EET plus I/R group; Phosphorylated ERK1/2 level was higher in I/R group than sham group, but was lower in I/R group than IP plus I/R group and EET plus I/R group; Phosphorylated p38 MAPK level was lower in control, sham, IP plus I/R and EET plus I/R group than I/R group. CONCLUSION: 11,12-EET protects rat heart against ischemia/reperfusion injury, the mechanism may be related to activation of ERK1/2 and inhibition of p38 MAPK. [

Aim To investigate the expression of phosphorylated JNK1/JNK2 and the protection of 11,12-EET in ischemic and reperfusion rat heart.Method The expression of JNK1/JNK2 was detected with western blot method and the changing of heart function during ischemia/reperfusion process was observed in different groups. Results The cardiac function (+dp/dt_(max)%,-dp/dt_(max)% and LVDP)of reperfusion periods(30 min) apparently decreased in ischemia/reperfusion (I/R) group contrasted with Sham group, short ischemia(SI)+I/R group and EET+I/R group,and the expression of phosphorylated JNK1/JNK2 increased in I/R group contrasted with nromal group,Sham group and EET+I/R group.Conclusion The myocardial protection of 11,12-EET ( 6.24?10~(-8) mol?L~(-1)) is able to inhibit the expression of phosphorylated JNK1/JNK2.

Objective To detect CYP2J3 gene expression and contents of 11,12-EET in heart,liver,lung,kidney and aorta thoracalis after CYP2J3 gene transfection.Methods The rat transgenic model was developed by injecting plasmid through vena dorsalis penis.The animals were divided into control group、 pcDNA3.1 transgenic group and pcDNA3.1-CYP2J3 transgenic group.The expression of CYP2J3 mRNA was detected by RT-PCR and content of 11,12-EET was examined by the HPLC at 14 days and 28 days after injection.Results Twenty eight days after injection,both expression of CYP2J3 mRNA and the content of 11,12-EET were significantly increased as compared with that of control and pcDNA3.1 transgenic group(P

AIM: To test the effect of ERK1/2 on ischemic preconditioning (IPC) in diabetic rat hearts. METHODS: The diabetic rat model was made with alloxan. After eight weeks, 24 rats were divided into 4 groups: non-diabetic IPC rats (group A); non-diabetic non-IPC rats (group B); diabetic IPC rats (group C); diabetic non-IPC rats (group D). ECGⅡ lead, left ventricular development pressure (LVDP), and first derivative of LVDP ~(?dp/dt_~max ) were recorded. Myocardial phosphorylation of extracellular signal regulated kinases1/2 (ERK1/2) was detected by Western-blotting. RESULTS: (1) The ventricular arrythmia score was significantly lower in group A than that in group C (P

AIM: In order to study the relationship of the activation of ERK and delayed cardioprotection of 11,12-EET.METHODS: A rat ischemia/reperfusion(I/R) model was replicated by ligating left anterior descending coronary artery 30 min followed by 60 min.The expression of ERK was detected with Western blotting,and the change of heart function during reperfusion was observed.RESULTS: The difference of myocardial function was prominent at (24 h) in I/R group compared with sham group,EET+I/R and EET+PD098059+I/R group.The activity of ERK at(24 h) in EET+I/R group was higher than sham group, and the activity of ERK in EET+PD098059+I/R group was lower than that in EET+(I/R) group;the expression of phosphorylated ERK1/ERK2 at(24 h) in EET+I/R group was more than that in I/R group,and the expression of phosphorylated ERK1/ERK2 in EET+PD098059+I/R group was less than EET+I/R group.CONCLUSION: 11,12-EET has a delayed cardioprotection effect,and this protection effect is involved in the activity of ERK and expression of phosphorylated ERK1/ERK2.

Objective To use the superior sagittal sinus (SSS) as an example to identify anatomical features of the bridging veins(BVs) draining into the SSS in both susceptibility weighted imaging (SWI) and three dimensional contrast enhancement MR venography (3D-CEMRV) images.Methods A total of 20 healthy volunteers (40 sides) were examined in this study.The venograms of each patient was obtained from SWI (40 sides out of 20 volunteers) and 3D-CE MRV (40 sides out of 20 volunteers).The data were analyzed by t test.Results According to their draining location with respect to the SSS,bridging veins were devided into two groups.Between the anterior group and the posterior group were two segments of the SSS into which few bridging veins drained.Observed by 3D-CE MRV and SWI,the average numbers of the anterior group were 1.9 ± 0.6 and 3.2 + 0.8,respectively,and the average diameters of the anterior group were (3.4 ± 1.1 ) and (2.1 +0.5 ) mm,respectively.These differences between 3D-CE MRV and SWI images were significant ( t =11.23,9.76,P ＜0.0l ).Observed by 3D-CE MRV and SWI,the average numbers of the posterior group were 3.5 + 1.2 and 5.9 ± 1.1,respectively,and the average diameters of the posterior group were ( 3.7 ± 0.9 ) and ( 2.9 ± 0.7 ) mm,respectively.The differences between the two technique were significant as well ( t =11.51,8.47,P ＜ 0.01 ).Conclusion The dural entrance of BVs into the SSS can be identified in both SWI and 3D-CE MRV images.The preoperative venogram by using 3D-CE MRV and SWI is useful to design a individual-tailored surgical approach for the preservation of BVs draining into SSS.SWI outweighs 3D-CE MRV in identifying anatomical features of the dural entrance of BVs into the SSS.

OBJECTIVETo isolate the side population (SP) and non-side population (NSP) cells from A431 cells and compare their difference in tumorigenicity in mice and the expression profiles of epithelial-mesenchymal transition (EMT) markers.

METHODSA431 cells stained with Hoechst 33342 were sorted with flow cytometry. The isolated SP cells and NSP cells were inoculated into NOD/SCID mice and the tumorigenicity of the cells was observed. EMT markers E-cadherin, β-catenin, vimentin, AXL, and Erbb3 in the tumor tissues were detected by immunohisto-staining.

RESULTSThe tumors generated by SP cells were larger than those by NSP cells in NOD/SCID mice. Compared with the tumors generated by NSP cells, the cells in the periphery of tumors generated by SP cells showed up-regulated expressions of AXL, vimentin and β-catenin and down-regulated ERBB3 and E-cadherin.

CONCLUSIONThe SP cells in A431 cells have a strong tumorigenicity and show more EMT phenotypes in tissues.

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