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1.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 385-390, 2010.
Article in Chinese | WPRIM | ID: wpr-349817

ABSTRACT

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.

2.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 745-749, 2009.
Article in Chinese | WPRIM | ID: wpr-341144

ABSTRACT

The single needle method for urethrovesical anastomosis with strengthened posterior fixation during laparoscopic radical prostatectomy was explored. The method was initiated by performing a fixing suture with a knot at 4 o'clock of the posterior lip of bladder neck,and another suture at nearby position was performed to leave the knot outside. From 5 o'clock to 8 o'clock,sutures were performed every one o'clock to secure posterior approximation,then every two o'clock a suture.To avoid a loose anastomosis,lock sutures were performed every 3 sutures. The needle was always driven full-thickness outside-in in the bladder neck and inside-out on the urethra. After completing the full circumference,the needle was drawn near the 4 o'clock and tied at the tail end. Any leakage could be closed with additional interrupted sutures. The clinical data of 89 patients who underwent this method were retrospectively compared with those of 23 patients who underwent the single knot method. The results showed that the anastomosis,operative and catheterization time was 17.6±4.7min,134.0±10.7 min and 6.5±1.6 days respectively. There were 3 temporal urinary leakages identified in 89 cases requiring prolonged catheterization. No urinary leak and anastomotic stricture was confirmed,and 95.2% patients had total urinary control. It was concluded that this method was simple and safe for urethrovesical anastomosis.

3.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 182-184, 2008.
Article in Chinese | WPRIM | ID: wpr-284613

ABSTRACT

To investigate the relationship between the expression of RASSFIA protein and promoter hypermethylation of RASSFIA gene, RASSFIA protein expression was measured by Western blot- ting in 10 specimens of normal bladder tissues and 23 specimens of bladder transitional cell carci- noma (BTCC). The promoter methylation in BTCC and normal bladder tissues was detected by me- thylation-specific PCR (MSP). The results showed that the expression level of RASSFIA protein was significantly lower in BTCC tissues than that in normal bladder tissues. However, it was not corre- lated with its clinical stages and pathological grades. The frequency of promoter methylation of RASSF1A gene was higher in BTCC tissues than that in normal bladder tissues. In 14 patients with the aberrant promoter methylation, 13 showed loss or low expression of RASSF1A protein. It is con- cluded that RASSFIA gene promoter methylation may contribute to the low level or loss of RASSFIA protein expression, the inactivation of RASSFIA gene and the genesis of BTCC. But, it may bear no correlation with its clinical stages and pathological grades.

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