Objective To study the puncture method of Angioseal closure device by femoral artery. Methods A prospective trial was carried out in 80 patients using Angioseal closure device in angiography and angioplasty. All patients were divided into tow groups, according to the horizontal distance between the entrance of skin and the entrance of the femoral artery: Group A, the distance 1.5 cm. Results 1. The rate of successful puncture was 92% in group A and 81% in group B (P

Objective To assess the safety and efficiency of Angioseal device in patients undergoing coronary percutaneous procedure.Methods A prospective trial was carried out in 260 patients undergoing angiograph and angioplasty during october 2002 to July 2003.All patients were divided into two groups: Angioseal closure device and manual compression.Results In angiography,the time to hemostasis was (1.8?0.9)min by Angioseal and (25.3?13.4)min by manual compression(P

Objective To evaluate the safety and feasibility of the implication of Cypher~(TM) drug-eluting stent in primary PTCA of acute myocardial infarction.Methods From November,2002 to November,2004,77cases of acute myocardial infarction patients enrolled into our hospital were treated by PCI within 12 hours after the heart attack.All patients were divided into two groups:Cypher~(TM) drug-eluting stent group(38) and conventional stainless steel stent group(39).Results The success rate of PCI were 100% in either group.38 Cypher~(TM) drug-eluting stent and 39 conventional stainless steel stent were implanted respectively.There was no significant difference in CAG result or clinical state among these two groups.Conclusion Cypher~(TM) drug-eluting stent can be safely and efficiently used in patients with acute myocardial infarction.

AIM: To investigate the effect of recombinant human interleukin-10 (rhIL-10) on IL-6 and TNF-? levels in serum and liver of mice exposed to lipopolysaccharide (LPS). METHODS: rhIL-10 was prepared by using genetic engineering technology. Mice were intraperitoneally with 500 ?g of LPS, and then were treated intravenously with various dosages of rhIL-10. The levels of IL-6 and TNF-? in hepatic tissue and serum were determined by ELISA at 12 h, 24 h, 48 h and 72 h post rhIL-10 treatment. RESULTS: rhIL-10 markedly inhibited the increase in IL-6 and TNF-? levels in hepatic tissue and serum at 12 h after rhIL-10 treatment in LPS-challenged mice, and the inhibition effect was significant at 24-48 h after rhIL-10 treatment (P

BACKGROUND:Restenosis and lumina loss limit further application of balloon extension and stent implantation.Effect of tunica intima proliferation and apoptosis in restenosis and the intervention method are exploring.OBJECTIVE:To investigate the influence of Rosuvastatin on the vascular smooth muscle cells proliferation and apoptosis in rats with carotid artery injury established by Medtronic balloon.METHODS:The male SD rats were randomly and equally divided into injury group and treatment group.Each rat was subjected to balloon injury on the lift common carotid artery,and control artery without balloon injury on the right artery served as control group.Treatment group rats were given Rosuvastatin(dissolved in Nacl)5 mg/kg per day 3 days before injury,while the injury group rats were given 9 g/L NaCl.At 7 and 14 days after injury,the common carotid arteries were harvested for HE staining.SM α-actin and proliferating celI nuclear antigen were detected by immunohistochemistry.In addition,smooth muscle cells apoptosis was detected by TUNEL.RESULTS AND CONCLUSION:The neointimal area and the area ratio of neointimal/media were decreased in treatment grouP significantly at 14 days compared with injury group(P<0.05),and neointimal area increased by 26%:positive cell rate of proliferating cell nuclear antigen was decreased,but apoptosis cells were increased cornpared with the injury group(P<0.05).Results showed that Rosuvastatin prior to balloon injury inhibited neointimal proliferation and neointimal celI proliferation following balloon Injury,promoted smooth muscle cells apoptosis,ultimately reducing neointimaI formation and inhibiting restenosis.

AIM: To observe the effects of H_2O_2 on apoptosis of skeletal muscle satellite cells (SMSC)and mitochondrial membrane potential (MMP), and protective effect of erythropoietin(EPO). METHODS: SMSC in vitro were divided into three groups: H_2O_2 group, H_2O_2+EPO group and control. Apoptosis rate and the means were obverted by monofluorescence flow cytometry. The morphological change of apoptosis cells were observed under fluorescence microscopy after Hoechst 33258 staining. RESULTS: The cells in H_2O_2 group show the highest apoptosis rate (22.13±1.79)%. In H_2O_2+EPO group, apoptosis rate were (16.47±2.53)%, (4.97±0.55)% and (2.93±0.47)% according to the EPO treated levels (10, 20 or 40 kU/L), respectively. MMP level in H_2O_2 group was the lowest 9.70±0.09. MMP levels in H_2O_2+EPO group were 12.67±0.32, 27.90±0.66, 44.53±0.93, respectively according to the EPO treated levels (10, 20 or 40 kU/L). In control group, apoptosis rate was 1.93±0.57 and MMP was 51.37±0.64. In H_2O_2 group and H_2O_2+ low dosage EPO group, Hoechst 33258 staining showed obvious apoptosis. CONCLUSION: EPO inhibits the apoptosis induced by H_2O_2 and stabilizes the MMP, which is related to the dosage of EPO.

BACKGROUND:Inflammation plays an important role in vessel proliferation after balloon injury.Reducing inflammatory reaction may lighten the ocurrence and development of the restenosis after angioplasty.Studies have demonstrated that PPAR? excitomotor has inhibitory effects on inflammation development.OBJECTIVE:To observe the changes in inflammatory factors after carotid artery balloon injury in rats and the intervention of PPAR? excitomotor rosiglitazone.DESIGN,TIME AND SETTING:The randomized,controlled animal experiment was performed at the Central Laboratory of Shenzhen People's Hospital from January to June 2009.MATERIALS:Male SPF SD rats weighing about 350 g were selected to generate models of carotid balloon injury.METHODS:SD rats were equally and randomly divided into 3 groups:the control group,the balloon injury group and the rosiglitazone group.The left common carotid arteries were injured by balloon in the balloon injury group and the rosiglitazone group.The control group received sham operation.The rosiglitazone group was administered rosiglitazone daily by gavage,which began 4 days before operation and continued until harvesting.Accordingly,the control group and the balloon injury group were administered normal saline daily by gavage.MAIN OUTCOME MEASURES:All rats were executed under anesthesia at 14 days after operation,respectively to harvest left common carotid artery samples.The vessels were stained by hematoxylin-eosin,and Neointimal area(NIA) and media area(MA) as well as NIA/MA were calculated.Real time RT-PCR and Western Blot method were used to assay the expression of interleukin(IL)-6,IL-10,IL-17A mRNA and the distribution of nuclear factor(NF)-?B protein.RESULTS:Of the 36 rats,5 were excluded due to failed modeling or death,and 31 rats were included in final analysis.①The expression levels of IL-6 and IL-17A mRNA in the rosiglitazone group were significantly lower than the balloon injury group,but higher than the control group(P

Objective:To detect and verifica the gene profile difference of microRNA-146a (miR-146a) and its role in the pro-liferation of vascular smooth muscle cells (VSMCs) by gene chip technology. Methods: Artificially synthesized miR-146a mimics(50 nmol/L) ,miR-146 inhibitor ( 50 nmol/L ) , scramble ( 50 nmol/L ) and PBS were transfected into cultured primary rat VSMCs in vitro. After transfection,Real time PCR was used to measure the levels of miR-146a and the cell counting kit 8(CCK8) was employed to investigate the proliferation of VSMCs. The VSMCs interfered by miR-146a inhibitor or miR-146a control were examined by gene chips and the profile of gene were analyzed by bioinformatics technology to detect the different genes and signal transduction pathway. The changes in mRNAs and proteins were accessed separately by Real time PCR and Western blot. Results: Compared with sham and control VSMCs,miR-146a expression level was significantly decreased in treatment with miR-146a inhibitor(P<0. 01),as well as optical density(OD) was also shown remarkably down regulated simultaneously(P<0. 05). The investigation of gene profile revealed that the p53 signal pathway was up-regulated in VSMCs interfered by miR-146a. The mRNA and protein expression levels of p53, caspase3 and PTEN in p53 signal transduction pathway didn′t show significant differences(P>0. 05),however,the mRNA and protein expression levels of cyclin D1 significantly increased in treatment with miR-146a mimics VSMCs group and decreased in miR-146a inhibitor VSMCs group ( compared with sham VSMCs group, both P<0. 05 ) . Conclusion: Our data indicated that miR-146a may promote the proliferation of rat VSMCs by up-regulating cyclin D1 expression.

BACKGROUND: Inflammation plays an important role in vessel proliferation after balloon injury. Reducing inflammatory reaction may lighten the ocurrence and development of the restenosis after angioplasty. Studies have demonstrated that PPAR_Y excitomotor has inhibitory effects on inflammation development. OBJECTIVE: To observe the changes in inflammatory factors after carotid artery balloon injury in rats and the intervention of PPARy excitomotor rosiglitazone. DESIGN, TIME AND SETTING: The randomized, controlled animal experiment was performed at the Central Laboratory of Shenzhen People's Hospital from January to June 2009. MATERIALS: Male SPF SD rats weighing about 350 g were selected to generate models of carotid balloon injury. METHODS: SD rats were equally and randomly divided into 3 groups: the control group, the balloon injury group and the rosiglitazone group. The left common carotid arteries were injured by balloon in the balloon injury group and the rosiglitazone group. The control group received sham operation. The rosiglitazone group was administered rosiglitazone daily by gavage,which began 4 days before operation and continued until harvesting.Accordingly,the control group and the balloon injury group were administered normal saline daily by gavage. MAIN OUTCOME MEASURES: All rats were executed under anesthesia at 14 days after operation, respectively to harvest left common carotid artery samples. The vessels were stained by hematoxylin-eosin, and Neointimal area (NIA) and media area (MA) as well as NIA/MA were calculated. Real time RT-PCR and Western Blot method were used to assay the expression of interleukin (IL)-6, IL-10, IL-17A mRNA and the distribution of nuclear factor (NF)-kB protein. expression levels of IL-6 and IL-17A mRNA in the rosiglitazone group were significantly lower than the balloon injury group, but higher than the Control group( P < 0.05), The expression levels of IL-10 mRNA in the rosiglitazone group were higher than the the rosiglitazone group was down-regulated, and lower than the balloon injury group, but higher than control group (P < 0.05). CONCLUSION: Rosiglitazone can regulate the expression of II-6 IL-10 IL-17A mRNA and the balance of inflammatory factors via NF-kB,inhibit the inflammatory reaction of injured vessels and may contribute to lighten the restenosis of injured vessels.

AIM:To investigate the proliferation property of stable chemerin gene knockdown vascular smooth muscle cells ( VSMCs) and to explore its mechanism .METHODS:The normal VSMCs , chemerin gene interfering control VSMCs and stable chemerin gene knockdown VSMCs were divided into normal group , PDGF group, control group and knockdown group .The VSMCs in PDGF group were given platelet-derived growth factor-BB ( PDGF-BB) to initiate proli-feration.The cell counting and BrdU assay were employed to investigate the proliferation property of VSMCs .The mitogen-activated protein kinase ( MAPK) signal pathway was determined by Western blot .RESULTS:The cell number and BrdU A value in PDGF-BB-treated VSMCs significantly increased as compared with the normal VSMCs ( P<0.05 ) .Compared with the normal VSMCs , the chemerin knockdown VSMCs showed obviously decreased cell number and BrdU A value ( P<0.05).Simultaneously, no significant difference in the proliferation of VSMCs between the normal VSMCs and the control VSMCs was observed.No significant difference of the protein levels of p-ERK1/2, ERK1/2, p-p38 MAPK and p38 MAPK among 4 kinds of VSMCs was found .The protein level of p-JNK in PDGF-BB-treated VSMCs was up-regulated, while it was down-regulated in chemerin knockdown VSMCs compared with the normal VSMCs .CONCLUSION: Chemerin pro-motes the proliferation of mouse vascular smooth muscle cells by up-regulating p-JNK production .