Objective To investigate the effect of survivin antisense oligodeoxynucleotides(ASODN) on(intimal) hyperplasia(IH) in vein graft in rats.Methods Autogenous vein graft model was established in 60 Wistar rats by transplanting the interior jugular vein to common jugular artery using microsurgical technique.The rats were divided into 5 groups according to different processing methods,including survivin ASODN 50?g and 200?g,scramble ODN 200?g,control group and lipoectin+pluronic group.Vein graft samples were harvested at 1 or 2 weeks after surgery and histomorphologic methods were used to compare the degree of IH.Survivin mRNA was measured by RT-PCR.Western blotting and immunohistochemistry methods also were used to detect the expression of survivin and PCNA.Apoptosis of VSMC was dectected by TUNEL.Results IH was evident within 1 to 2 weeks after vein grafting,but was markedly inhibited by 50?g of survivin ASODN(P

Objective To study the effect of antisense RNA retroviral vector of mTOR on the proliferation of vascular smooth muscle cells(VSMC).Methods The conservative region of mTOR gene was inserted into pLXIN reversedly,then the vector was packaged in PT67 cells by transfection with lipofectamine and(transfected) to VSMC.The efficiency of antisense inhibition was verified,and the changes of p70S6k and(4E-BP1) were also determined at the same time.The proliferation activity was determined by flowcytometry and MTT.Results After the vector was successfully transfected to the cells.pLXIN-A-mTOR vector could(efficiently) decrease mRNA and protein expression of mTOR and p70S6k of the cell,while the expression of 4E-BP1 increased significantly.The cell cycle and proliferation activity of VSMC was also stunned in phase G_1.Conclusions The mTOR antisense retroviral vector,pLXIN-A-mTOR,has been constructed(successfully),which can significantly inhibit the proliferation of VSMC.

Objective To study the expression of mammalian target of rapamycin (mTOR) in autogenous vein graft. Methods Autogenous vein graft model was established in 64 Wistar rats. Graft vein was harvested 6 hours, 1 day, 3 days, 1 week, 2 weeks, 4 weeks, 6 weeks and 8 weeks after transplantation. mTOR mRNA was measured by RT-PCR and in situ hybridization. Western blotting and immunohistochemistry methods were used to detect the expression of mTOR. PCNA expression was detected. Results The vein graft mRNA and protein expression of mTOR increased soon after transplantation. mTOR mRNA reached the peak 1 to 2 weeks after surgery [(48?18)% and (33?11)% respectively, P

Objective To investigate the expression of Notchl and NUMB in gastric cancer and explore the relationship between two genes and clinicopathologic features. Methods The mRNA and protein expressions of Notchl and NUMB in the gastric cancer tissues and normal gastric tissues were determined by realtime PCR and Western blotting. Results The mRNA expression of Notchl in gastric cancer tissues was 1.67times that of Notchl in normal gastric tissues. The increase of the mRNA expression of Notchl was correlated with tumor differentiation and lymph node metastatis of the patients ( P < 0. 05 ). The mRNA expression of NUMB in gastric cancer tissues was 0.597 times that of Notchl in normal tissues. The decrease of the mRNA expression of NUMB was correlated with tumor differentiation of the patients (P < 0.05). The expression of Notchl was negatively correlated to that of NUMB ( r = - 0.459, P < 0.05 ). The protein expression of Notchl in gastric cancer tissues was (0. 348 ±0. 133) , which was significantly higher than (0. 208 ±0. 140) in normal gastric tissues (P < 0.05 ). The protein expression of NUMB in gastric cancer tissues was (0.490 ±0.440), which was significantly lower than 0.746 ±0.390 in normal gastric tissues (P<0.05).Conclusion Up-regulation of Notchl and down-regulation of NUMB may play an important role in the occurrence and development of gastric cancer.

Objective To study the expression of hypoxia-inducible factor(HIF)-1? and related genes in ruptured abdominal aorta aneurysm(RAAA) and explore the underlying pathogenesis. Methods 18 RAAA specimens were collected and 20 AAA tissues were used as control. Total RNA was extracted and Northern blot was used to evaluate the expression of HIF-1? mRNA. Western blot and immunohistochemistry method were used to determine the expression of HIF-1? and vascular endothelial growth factor(VEGF). Microvessel density(MVD) was measured for CD34. Results The expression of HIF-la mRNA was significantly higher in RAAA than that in AAA (P

Objective To investigate the expression and relationship of early growth response gene-1((Egr-1)),platelet-derived growth factor-B(PDGF-B) and tranforming growth factor(TGF-?_1) in autogenous vein graft in rats,and the role in vein graft intimal hyperplasia(IH).Methods Autogenous vein graft model was(established) in 90 wistar rats.The vein graft samples were harvested at 1,2,6,24 hours,and 3,7,14,28,42 days after surgery.Normal vein was used as control group.Egr-1、PDGF-B,TGF-?_1 mRNA was measured by reverse transcription-PCR and in situ hybridization.Western blotting and immunohistochemistry were used to detect the protein expression of Egr-1,PDGF-B and TGF-?_1. Results Expression of Egr-1,PDGF-B,TGF-?_1 mRNA and protein was not detected in normal vein.In grafting vein,expression level of Egr1mRNA reached a peak at 28days,and the positive rate of Egr-1mRNA was 45%?6%;(PDGF-BmRNA) reached a peak at 14days(48%?6%);a peak of TGF-?_1mRNA was 46%?9% reached at 7days;Egr-1 protein expression reached a peak at 28days, and the positive rate of Egr-1 protein was 40%?9%.PDGF-B protein reached a peak at 28days(45%?4%),TGF-?_1 protein reached a peak at 14days(41%?7%).Conclusions Intimal hyperplasia of vein graft is closely associated withexpression of Egr-1、PDGF-B and TGF-?_1;the activation and expression of PDGF-B and TGF-?_1 may be(modulated) by Egr-1,and they may contribute to increase expression of Egr-1 by feedback.

Objective To study the effect of antisense mTOR gene transfection mediated by nanoparticles(NP) on intimal perliferation after vein grafting.Methods Nanoparticle antisense mTOR gene complex was prepared with PLGA and PVA.Autogenous vein graft model was established in 72 rats by transplanting internal branch of jugular vein to carotid artery.Three groups were studied:(1) antisense mTOR group,antisense mTOR gene mediated by NP was transfected into the veins before anastomosis.(2) Empty vector group,the vein was transfected by empty vector mediated by NP.(3) Control group,no transfection.The grafted veins were harvested 3 days,1 week,2 weeks and 4 weeks after operation,respectively.The exogenous mTOR mRNA and protein expression were determined and intimal hyperplasia(IH) was observed.The presence of apoptotic VSMC was also detected.Results Antisense mTOR gene transfection mediated by nanoparticle complex inhibited the mRNA and protein expression of mTOR gene(P

Objective To study the expression of mammalian target of rapamycin(mTOR)in ischemic postconditioning(I-postC)-induced attenuation of ischemia/reperfusion(I/R)injury in rat skeletal muscle.Methods A total of 48 healthy male Wistar rats were randomly divided into 3 groups(n=16 each group):I/R group(4-hour ischemia followed by 12-or 24-hour reperfusion),ischemic preconditioning (IPC)group(3 cycles of 5-minute ischemia followed by 5-minute reperfusion),and I-postC group(3 cycles of 1-minute reperfusion followed by 1-minute ischemia).The rat model of I/R injury in right hind limb model was established by clamping the right femoral artery.The changes in the morphology,wet-to-dry weight ratio(W/D),malondialdehyde(MDA),and myeloperoxidase(MPO)in skeletal muscle were compared.The expression of mTOR was detected by Western blot and immunohistochemistry.Results In I-postC and IPC groups,the skeletal muscle edema was less severe,the levels of MDA and MPO significantly decreased,and the expression of mTOR significantly in creased,compared with I/R group(all P＜0.03).There was no significant difference between I-postC and IPC groups.Conclusion Ipostc may attenuate I/R injury in rat hind limbs by activating mTOR signal pathway,which is similar to the mechanism of IPC.

Objective To investigate the prevalence rate of hypertension among the elderly population in Shanxi Province. Methods According to the random sampling, 41 residents committees of city blocks and villages of 9 areas (including Taiyuan, Datong, Jinzhong, Yuncheng, et al) of Shanxi Province were extracted as the investigative spots. All the people were older than 55years, and risk factors for hypertension were identified. Results A total of 3702 people were surveyed, including 1,782 men and 1,920 women. The total hypertension prevalence rate was 39.0%(the standardized rate: 39. 5 %), with 38. 7 % in men (the standardized rate: 38. 5%), 39.3 % in women (the standardized rate: 41.2%), and no statistic significance was found between men and women (χ2= 0. 143, P>0. 05). Aging, lacking of knowledge, and obesity were risk factors for hypertension. Conclusions The hypertension in Shanxi Province has a high prevalence rate among the elderly population, a comprehensive intervention should be taken in the prevention of hypertension.

This study was to investigate the protective effects of Jinqi Jiangtang tablets on diabetic complications of cardiovascular disease in Drosophila. The effects of Jinqi Jiangtang tablets on hypolipidemia and hypoglycemia by high fat diet(HFD)induced model organism Drosophila with the content of triglyceride and trehalose in Drosophila as indexes, were investigated. And the Drosophila heart function was detected by high speed EM-CCD; cell signaling pathways were detected by Western blot and RT-PCR. The results showed that high fat diet could induce the appearance of hyperglycemia and hyperlipidemia on Drosophila model. Jinqi Jiangtang tablets could significantly reduce triglyceride and trehalose and protect heart function of Drosophila induced by high fat diet. Jinqi Jiangtang tablets could also increase the expression of 4ebp mRNA, while decreasing p-4EBP protein and pepck mRNA expression. This study demonstrated that Jinqi Jiangtang tablets have a protective effect on HFD-induced dyslipidemic-diabetic and cardiac dysfunction, which may be related to mTOR/4EBP pathway.