Objective To study the value of imaging characters in diagnosing mediastinal tumors.Methods X-ray and CT findings of pathologically proved mediastinal tumors in 58 cases were analysed,the findings enabling qualitative diagnosis were recommended. Results There were 40 cases of anterior mediastinal tumors including intrathoracic thyroid tumors [n=32,5 tyroid carcinomas and 1 thyroid cyst ,thymomas (n=3) and teratomas (n=5, 3 cases ruptured)]. All the other 18 cases in posterior mediastinum were neurogenic tumors.Conclusion Based on the combination of the mediastinal compartment knowledge, X-ray and CT findings of the tumors and the clinical information, the qualitative diagnosis of mediastinal tumors will be characterized correctly.

AIM:To evaluate the effects of atorvastatin on nitric oxide(NO),endothelin-1(ET-1)and myocardial no-reflow in a rabbit model of acute myocardial infarction and reperfusion(AMI/R). METHODS:Twenty-four rabbits were randomized into 3 groups:8 in AMI/R group,8 in atorvastatin-treated group(5 mg·kg~(-1)·d~(-1))and 8 in sham-operated group. Animals in the former two groups were subjected to 60 min of coronary occlusion followed by 120 min of reperfusion. Data on haemodynamics were collected. NO in blood sample,and in normal,and in infarcted reflow and no-reflow myocardium were evaluated respectively by nitrate reductase method. The levels of ET-1 in blood sample,and in normal,infarcted reflow and no-reflow myocardium were determined by radioimmunoassay. RESULTS:(1)Compared to the baselines,the heart rate(HR),systolic blood pressure(SBP),diastolic blood pressure(DBP),left ventricular systolic pressure(LVSP),maximal rate of increase and decline in left ventricular pressure(±dp/dt_(max))and cardiac output(CO)in AMI/R and atorvastatin-treated groups were significantly declined,whereas left ventricular end-diastolic pressure(LVEDP)was increased after 60 min of coronary occlusion and 120 min of reperfusion(P<0.05 or P<0.01). However,in atorvastatin-treated group,LVSP,LVEDP,±dp/dt_(max) and CO at the time point of 120 min of reperfusion recovered more significantly than those at the time point of 60 min of coronary occlusion(P<0.01),which was more significant than those in AMI/R group(P<0.05 or P<0.01). Compared to AMI/R group,the SBP and DBP were significantly heigher in atorvastatin-treated group(P<0.01).(2)In atorvastatin-treated group,the levels of ET-1 in blood sample were significantly lower than those in AMI/R group(P<0.01),and the levels of NO were significantly higher(P<0.01). Moreover,the levels of NO or ET-1 in infarcted reflow myocardium were significantly lower than that in AMI/R group(P<0.05 or P<0.01).(3)Atorvastatin could ameliorate myocardial function. CONCLUSION:Atorvastatin is effective in increasing NO and reducing ET-1 in blood plasma and local myocardium,and in protection of endothelial cells. Atorvastatin also has a beneficial effect on improving left ventricular function during acute myocardial infarction and reperfusion in rabbits.

Objective　To study the effect on the proliferation of vascular smooth muscle cells(VSMC) after transferring angiotensin Ⅱ(AngⅡ) type 2 receptor(AT2R) gene.Methods　The recombinant adenoviral vector AdcCMV-AT2R, containing rat AT2 receptor gene which was constracted by homologous recombination, was used to transfer AT2 receptor gene to rat VSMC in vitro. The expression of AT2R mRNA was detected by RT-PCR. The rate of expression and the change of cell cycle in VSMC were analysed by flow cytometry. Cell devision index, incorporation of bromodeoxyuridine(BrdU)and 3-(4,5-dimethyl-thiazol-2-yl)2,5-diphenytetrazolium bromide(MTT) were used to determine the proliferation of VSMC, respectively.Results　RT-PCR showed that the expression of AT2R mRNA increased obviously in transferred VSMC, and the peak value of expression rate was about 89.51% at 48 hours. When the expression of AT2R was at peak value, the ratio of S and G2-M periods was reduced from 31.7% to 13.9%(P<0.05) and the index of cell division from 37.4% to 9.6%(P<0.01). The OD values of MTT and BrdU incorporation were reduced by 61.4% and 51.6% respectively(P<0.01).Conclusion　Our study indicates that AdCMV-AT2R can generate high level expression of AT2 receptor in cultured rat VSMC and its expression can significantly inhibit the proliferation of rats VSMC in vitro. It may be a new selection for the gene therapy of restenosis after angioplasty.

Objective Overexpressing gax gene in vascular smooth muscle cells(VSMC) mediated by adenovirus transfection.Methods Replication defective adenovirus type 5 (Ad5) vector encoding the rat gax gene (AdCMV gax) was constructed via site specific recombination and amplified in 293 cells. The resulting adenovirus was purified for a high viral titer. The expression of gax mRNA and protein was evaluated by a series of methods such as reverse transcription polymerase chain reaction (RT PCR), flow cytometry and immunocytochemical technique after gax gene was transferred to VSMCs. Results When AdCMV gax was transfected to VSMCs, the expression of gax protein increased significantly in VSMCs, and reached 80% in 24 hours. High expression of gax protein could keep for over 5 days. Before AdCMV gax was transfected to VSMCs, gax mRNA and protein could be down regulated by platelet derived growth factor (PDGF) BB. After AdCMV gax was transfected to VSMCs, the level of gax expression was significantly higher than that before transfection, and no correlation with the stimulation of PDGF BB.Conclusions gax gene can be transfected to VSMC by AdCMV gax and translated to protein, which is advantageous to exploring the effects of gax gene on biological behaviour of VSMC.

AIM:To evaluate the effects of atorvastatin on nitric oxide(NO),endothelin-1(ET-1)and myocardial no-reflow in a rabbit model of acute myocardial infarction and reperfusion(AMI/R). METHODS:Twenty-four rabbits were randomized into 3 groups:8 in AMI/R group,8 in atorvastatin-treated group(5 mg?kg-1?d-1)and 8 in sham-operated group. Animals in the former two groups were subjected to 60 min of coronary occlusion followed by 120 min of reperfusion. Data on haemodynamics were collected. NO in blood sample,and in normal,and in infarcted reflow and no-reflow myocardium were evaluated respectively by nitrate reductase method. The levels of ET-1 in blood sample,and in normal,infarcted reflow and no-reflow myocardium were determined by radioimmunoassay. RESULTS:(1)Compared to the baselines,the heart rate(HR),systolic blood pressure(SBP),diastolic blood pressure(DBP),left ventricular systolic pressure(LVSP),maximal rate of increase and decline in left ventricular pressure(?dp/dtmax)and cardiac output(CO)in AMI/R and atorvastatin-treated groups were significantly declined,whereas left ventricular end-diastolic pressure(LVEDP)was increased after 60 min of coronary occlusion and 120 min of reperfusion(P

Objective To investigate the role of intracellular protein tyrosine kinase (PTK) activation in vascular smooth muscle cells (VSMCs) migration mediated by angiotensin Ⅱ (AngⅡ). Methods Intracellular PTK activities were investigated by means of ?- 32 P incorperation in cultured rat VSMCs stimulated by AngⅡ. The migrated VSMCs were enumerated in a modified Boyden Chamber. Results Without any specific stimulus, only a few migrated cells were detected. However, the number of migrated cells were increased, under the condition of AngⅡ at the concentration of 1?10 -10 , 1?10 -9 , 1?10 -8 , 1?10 -7 and 1?10 -6 mol/L, by 3.7, 4.6, 5.9, 6.6 and 6.3 times respectively, compared with the control group. Intracellular PTK activities were also increased by 1.0,1.7,2.4,3.2 and 2.4 times compared with the control group, under the condition of AngⅡ at the concentration of 1?10 -10 , 1?10 -9 , 1?10 -8 , 1?10 -7 and 1?10 -6 mol/L, respectively. Statistical analysis showed that there was a significant positive correlation between AngⅡ-induced VSMCs migration and intracellular PTK activation. Correspondingly, PTK inhibitor Genistein significantly reduced AngⅡ-induced VSMCs movement ( P

Objective To study the effect of rat angiotensin Ⅱ receptor (AT2R) gene transfer mediated by adenoviral vector on neointimal proliferation after rat carotid artery injury. Methods AT2R gene was transducted into the carotid artery by adenoviral vector with GFP after carotid balloon injury. Restenosis models were established in Wistar rats. Immunostaining was performed to examin the expression of AT2R in local arteries. Neointima/media area ratio at day 21 after gene transfer was measured by morphometric analysis. Results The transduction rate of AT2R gene in rat carotid arteries was 40% and the gene expressed constantly in the vessel walls. Neointima/media area ratio of the gene transduction group was significantly reduced (48%) compared with the control group at day 21 after gene transfer. Conclusion The results suggest the possibility that AT2R gene transfer can inhibit proliferation of arterial intima after balloon injury and it is a potential therapeutic approach to prevent neointimal hyperplasia.

Objective To study the change of the expression of cellular growth factor receptor and its effect on the proliferation and migration of vascular smooth muscle cells (VSMCs) under electrical field. Methods 1) A electrophoresis apparatus was designed for applying the direct current electric fields to the cultured VSMCs, which were separated from the aorta of rats. Interval photographs were used to analyse the direction and distance of VSMCs migration. Cellular growth factors such as platelet derived growth factor receptor (PDGFR), angiotensin II type 1 receptor (AT1R) and its type 2 receptor(AT2R) were studied by immunohistochemistry or immunofluorescence to show the mechanism relation to the migration of VSMCs. Results Under the direct current electric field, the expression of PDGFR was increased obviously and distributed asymmetricly on the membrane of VSMCs. The receptor mainly focused on the cathode side of cellular membrane in electric field. The AT1R were also enhanced in the cells after exposure to the electric field, but the expression of AT2R was uncharged. The longer exposure time to the 150 mV/mm electric field, the more electrotaxis the cells showed. The distance of cellular migration increased obviously with the time to exposure the electric field comparing with the control group. There was no significant difference in the expression of proliferating cell nuclear antigen (PCNA) between two groups. Conclusion External electric fields applying to the rat VSMCs can change the growth characteristic and enhance directional migration of VSMCs. These effects maybe related to the up-regulated expression and re-distribution of some cellular growth factors such as PDGFR, AT1R and AT2R.

Objective: To construct recombinant adenovirus vector of Antisense BTEB2 cDNA and study the effect of antisense BTEB2 on proliferation of vascular smooth muscle cells and neointimal hyperplasia.Methods:BTEB2 cDNA was prepared by RT PCR technique and was subcloned reversedly into shuttle plasmid pDC315 to constructed recombinant shuttle plasmid pDC315AS BTEB2.Then the recombinant shuttle plasmid and adenovirus genomic plasmid pBHGlox?E1,3Cre were cotransfected into 293 cell to obtain recombinant adenovirus. The PCR technique was used to detect target gene fragment and adenovirus genomic characteristic fragment. After the recombinant adenovirus infected vascular smooth muscle cells, antisense RNA expression of BTEB2 was detected by RT PCR. Results:There was recombinant adenovirus containing BTEB2 cDNA in the lysate of cotransfected 293 cells.The recombinant adenovirus infected 293 cells and replicated in 293 cells. The expression of BTEB2 antisense RNA was very obvious in vascular smooth muscle cells after infected by recombinant adenovirus. Conclusion:The construction of recombinant adenovirus vector of Antisense BTEB2 has been achieved, and Antisense RNA of BTEB2 can express in vascular smooth muscle cells. This study has paved the way for furthur research.

Objective To investigate the mechanism of affecting smooth muscle cells apoptosis after balloon injury to vessel Methods The percentage of vascular smooth muscle cells (VSMC) apoptosis and the expression of angiotensin Ⅱ subtype 1 receptor (AT 1R) was measured by terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labeling (TUNEL) and immunohistochemical technique after balloon injury Results Compared with sham's, the expression of AT 1R protein in vascular media was significantly increased at 3 days after balloon injury ( P