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1.
China Journal of Endoscopy ; (12): 11-15, 2017.
Artigo em Chinês | WPRIM | ID: wpr-613608

RESUMO

Objective To explore the clinical safety and efficacy of self-made single-port retroperitoneoscopic renal pedicle lymphatic disconnection for chyluria. Methods From Feb 2013 to Mar 2016, clinical data of 34 patients were collected. Of them, 16 cases underwent self-made single-port retroperitoneoscopic renal pedicle lymphatic disconnection and 18 cases underwent three port retroperitoneoscopic renal pedicle lymphatic disconnection. No significant difference was shown in age, body mass index between the two groups (P > 0.05). Mean operative time, estimated bleeding volume, drainage time, postoperative hospital stay, postoperative pain evaluation, satisfaction scores of incision were compared between the two groups. Results All procedures were successfully performed without conversion to open surgery. Compared with the three port surgery group, results in the single-port group were superior in terms of mean operative time [(102.3 ± 16.1) versus (132.4 ± 21.6) min, P < 0.05], there were no significant differences in estimated blood loss, drainage time, postoperative hospital stay, the date in postoperative pain evaluation, satisfaction scores of incision shown that single-port group was superior to three port group. Conclusion Our initial experience revealed that single-port retroperitoneoscopic renal pedicle lymphatic disconnection was a safe, effective, cost-effective and less-invasive procedure for chyluria with improved postoperative pain and cosmetic results.

2.
Chinese Journal of Pathophysiology ; (12)2000.
Artigo em Chinês | WPRIM | ID: wpr-522957

RESUMO

AIM: To investigate molecular mechanisms associated with the acquisition of androgen-independent growth of human prostate cancer during progression. METHODS: Upon continuously passaging, the androgen-independent LNCaP cell model was established. The expression of AR and PSA proteins in the course of prostate cancer progression was determined by Western blot. RESULTS: Upon continuous passage, the biological behavior of androgen-dependent parental LNCaP C-33 cells (passage number less than 33) was altered. LNCaP C-81 cells (passage number higher than 80) exhibited more aggressive growth and lower androgen-dependence than C-33 and C-51 cells (passage number between 33 and 80). C-81 cells secreted a higher level of PSA and the degree of DHT stimulation on PSA secretion was lower in C-81 cells than C-33 cells. The three LNCaP subclones expressed a similar level of total AR protein, but C-81 cells showed a characteristic loss of expression of the AR-B and increase in expression of the AR-A. CONCLUSION: Multiple factors, including the different expression of AR isoforms, contribute to the development of androgen-independent growth of prostatic carcinoma cells. [

3.
Chinese Journal of Urology ; (12)1994.
Artigo em Chinês | WPRIM | ID: wpr-539083

RESUMO

Objective To establish and validate andro ge n-independent human prostate cancer LNCaP cell model. Methods Androgen-dependent LNCaP parental C-33 cells were maintained in a regul ar cell-culture medium,that is,phenol red-positive RPMI 1640 medium supplement ed with 10% fetal bovine serum,1% glutamine and 0.5% gentamicin.Upon continuousl y passaging,androgen-dependence of these LNCaP cells decreased gradually,thus,t he androgen-independent LNCaP cell model which derived from androgen-dependent cells was established. Results Upon continuous passage, the biological behavior of androgen-dependent parental LNCaP C-33 cells (pass age number less than 33) was altered.LNCaP C-81 cells (passage number higher th an 80) clearly exhibited more aggressive growth and lower androgen-dependence t han C-33 and C-51 cells (passage number between 34 and 81) in vitro and in viv o. Conclusions The LNCaP cell model closely recapitulate s the transition of human prostate cancer from androgen-dependent to hormone-r efractory state under the androgen nondeprived condition. This cell model may pr ovide the opportunity to understand the molecular mechanisms involved in the and rogen-independent growth of cancer cells during prostate cancer progression.

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