Objective To assess the results of emergency endovascular stent-grafting for patients with acute Stanford type B aortic dissection(type B AAD)within 24 hours of onset.Methods Between June 2007 and October 2008,30 patients with acute type B aortic dissection underwent emergency endOVascular stent-grafting within 24 hours of presentation.Under general anesthesia,stent-graft was deploved at the proper position of first tear entry through femoral artery under X-ray monitering.Follow-up by CT was performed 1 w,1 m ,3 m,6 m,1 y postoperatively to observe the efficacy and complications such as endoleak,migration and fracture of stent-graft. Result The technical success rate was 100%;13.4%(4 cases) endoleak rate was identified immediately after deployment.Follow up was made between 1 month to 19 months,averaging at(12±8)months,3.3%type-1 endoleak Was observed after 6 months;One patient died within 30 days possibly of dissection rupture;One patient died of acute liver failure during the follow-up. Conclusion Endovascular repair with stent-graft within 24 hours of presentation was effectivefor the treatment of acute type B aortic dissection.

Objective To study the role of fibulin-5 in urothelial carcinoma of bladder. Methods Fibulin-5 expression was detected in bladder cancer tissues (13 cases of G_1 and G_2, 7 cases of G_3) and normal bladder mucosa samples by Western blotting assay. Fibulin-5 cDNA was amplified by PCR and cloned into pMD-19T simple vector. The pMD-19T-Fibulin-5 vector was digested by restriction endonucleases XhoI and EcoRI to generate a XhoI-Fibulin5-EcoRI fragment that was then ligated into the identical sites in p-EGFP-Nl plasmid to synthesize p-EGFP-Fibulin-5 plasmid. The p-EGFP-Fibulin-5 plasmid was finally transfected into bladder cancer cell line 5637. The migration and invasion of untransfected, vector-transfected and fibulin-5-transfected bladder cancer cells were measured by Boyden chamber assay. Results Compared to 1. 16 ±0. 28 in the normal control, the expression of fibulin-5 protein in low grade and high grade tumors were 0. 57±0. 32 and 0. 44±0. 42(P<0. 01, respectively). However, the difference between low grade and high grade tumors was not statistically significant (P>0. 05). The successfully transfected bladder cancer cells demonstrated green fluorescent light. The migrated cell number of fibulin-5-transfected cells was 127. 6 ± 3. 1 compared with 139. 3±7. 7 for vector-transfected cells and 136. 9±5. 7 for untransfected cells (P>0. 05, respectively). In contrast, the invaded cell number of fibulin-5-transfected cells was 8. 0±3. 1 compared with 31. 5±4. 8 for vector-transfected cells and 31. 7±4. 7 for untransfected cells (P<0. 01, respectively). Conclusion Fibulin-5 is down-regulated in urothelial carcinoma of bladder and acts as a tumor suppressor gene by inhibiting the invasion of bladder cancer cells.

This study aimed to determine whether aldosterone could induce vascular cell apoptosis in vivo. Thirty-two male rats were randomly divided into 4 groups: vehicle (control), aldosterone, aldosterone plus eplerenone or hydralazine. They were then implanted with an osmotic mini-pump that infused either aldosterone or the vehicle. Systolic blood pressure (SBP) was measured weekly by the tail-cuff method. After 8 weeks, plasma aldosterone concentration (PAC) and renin activity (PRA) were determined by radioimmunoassay. Aortic apoptosis was examined by TUNEL assay. The levels of cytochrome c and caspase-3 were determined by Western blotting and the expression of Bax and Bcl-2 was detected by immnuohistochemistry and Western blotting. The results showed that as compared with control group, aldosterone-infused rats exhibited: (1) an increase in SBP; (2) significantly elevated PAC with depressed PRA; (3) elevated aortic vascular cell apoptosis accompanied with higher levels of cytochrome c and activated caspase-3; and (4) significantly up-regulated Bax protein with down-regulated Bcl-2. These effects of aldosterone were significantly inhibited after co-administration with eplerenone but not with hydralazine. It was concluded that aldosterone induced vascular cell apoptosis by its direct effect on the aorta via mineralocorticoid receptors and independently of blood pressure, which may contribute to aldosterone-mediated vascular injury.

This study aimed to determine whether aldosterone could induce vascular cell apoptosis in vivo.Thirty-two male rats were randomly divided into 4 groups: vehicle(control),aldosterone,aldosterone plus eplerenone or hydralazine.They were then implanted with an osmotic mini-pump that infused either aldosterone or the vehicle.Systolic blood pressure(SBP)was measured weekly by the tail-cuff method.After 8 weeks,plasma aldosterone concentration(PAC)and renin activity(PRA)were determined by radioimmunoassay.Aortic apoptosis was examined by TUNEL assay.The levels of cytochrome c and caspase-3 were determined by Western blotting and the expression of Bax and Bcl-2 was detected by immnuohistochemistry and Western blotting.The results showed that as compared with control group,aldosterone-infused rats exhibited:(1)an increase in SBP;(2)significantly elevated PAC with depressed PRA;(3)elevated aortic vascular cell apoptosis accompanied with higher levels ofcytochrome c and activated caspase-3; and(4)significantly up-regulated Bax protein with down-regulated Bcl-2.These effects of aldosterone were significantly inhibited after co-administration with eplerenone but not with hydralazine.It was concluded that aldosterone inducedvascular cell apoptosis by its direct effect on the aorta via mineralocorticoid receptors and independently of blood pressure,which may contribute to aldosterone-mediated vascular injury.