Penile necrosis resulting from post-circumcision microwave diathermy: A report of 9 cases / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the pathogenesis and treatment of penile necrosis resulting from microwave diathermy following circumcision.</p><p><b>METHODS</b>We retrospectively analyzed the clinical data about 9 cases of penile necrosis resulting from postoperative microwave diathermy following circumcision. The 9 males, aged 20 - 39 (mean 26) years, underwent traditional circumcision for redundant prepuce or phimosis in other hospitals, followed by microwave diathermy for 30 - 60 minutes daily, which resulted in penile necrosis. With no response to conservative therapy, the patients were referred to our hospital at 3 -30 days postoperatively. Of the 9 patients, 5 presented with dry gangrene and 4 with moist gangrene. Six of the patients underwent partial penectomy, including 1 that received penis lengthening.3 months later, while the other 3 underwent total penectomy for total penile necrosis followed by penile reconstruction 3 months later, with deep inferior epigastric perforator (DIEP) flaps and by implantation of the 12th costal cartilage in 2 cases and with epigastric groin island flaps and by urethroplasty in the other.</p><p><b>RESULTS</b>The patients were followed up for 2 - 8 years, and all could urinate smoothly in the standing position. Of the 6 men treated by partial penectomy, 1 received penis lengthening and achieved a penile length of 7 cm and 5 had the remaining penile length of 3 -5 cm, 4 with erectile function and the other 2 capable of sexual intercourse. The 3 men treated by total penectomy achieved nearly normal external appearance of the penis, with a finalized length of (11.7 ± 1.3) cm, a circumference of (11.4 ± 2.1) cm, and a normal feel of the skin. Of the 3 cases of penile reconstruction, 2 achieved sufficient erectile hardness of the penis (grade 3) for sexual intercourse, while the other 1 remained impotent.</p><p><b>CONCLUSION</b>Post-circumcision microwave diathermy may result in penile necrosis, for the management of which, early debridement is necessitated and penile lengthening or reconstruction can be performed according to the severity of the lesion and needs of the patient.</p>

Monitoring of prostate cancer growth and metastasis using a PSA luciferase report plasmid in a mouse model

OBJECTIVE@#To construct a PSA luciferase report plasmid and monitor the growth and metastasis of prostate cancer after emasculation in SCID mice.@*METHODS@#PSA promoter sequence and luciferase gene were amplified by PCR and subsequently inserted into pZsGreen1-1 vector to construct pPSA-FL-Luc vector. LNCaP cells that were stably transfected with pPSA-FL-Luc were used to establish a SCID mouse xenograft model. Then, the growth and metastasis of prostate cancer were monitored via living imaging.@*RESULTS@#We successfully constructed a PSA luciferase plasmid, pPSA-FL-Luc. DHT enhanced luciferase activity in a concentration-dependent manner in 293T cells with pPSA-FL-Luc transfection. Prostate cancer SCID mouse model was established with pPSA-FL-Luc transfected LNCaP cells. In tumor bearing mice with or without emasculation, pPSA-FL-Luc plasmid was applied to monitored tumor growth and metastasis based on bioluminescence imaging.@*CONCLUSIONS@#We construct a pPSA-FL-Luc plasmid, which stably expresses luciferase and can be applied to monitor tumor development in a prostate SCID mouse model.

Monitoring of prostate cancer growth and metastasis using a PSA luciferase report plasmid in a mouse model

Objective: To construct a PSA luciferase report plasmid and monitor the growth and metastasis of prostate cancer after emasculation in SCID mice. Methods: PSA promoter sequence and luciferase gene were amplified by PCR and subsequently inserted into pZsGreen1-1 vector to construct pPSA-FL-Luc vector. LNCaP cells that were stably transfected with pPSA-FL-Luc were used to establish a SCID mouse xenograft model. Then, the growth and metastasis of prostate cancer were monitored via living imaging. Results: We successfully constructed a PSA luciferase plasmid, pPSA-FL-Luc. DHT enhanced luciferase activity in a concentration-dependent manner in 293T cells with pPSA-FL-Luc transfection. Prostate cancer SCID mouse model was established with pPSA-FL-Luc transfected LNCaP cells. In tumor bearing mice with or without emasculation, pPSA-FL-Luc plasmid was applied to monitored tumor growth and metastasis based on bioluminescence imaging. Conclusions: We construct a pPSA-FL-Luc plasmid, which stably expresses luciferase and can be applied to monitor tumor development in a prostate SCID mouse model.

Casticin induces caspase-mediated apoptosis via activation of mitochondrial pathway and upregulation of DR5 in human lung cancer cells

OBJECTIVE@#To assess if casticin induces caspase-mediated apoptosis via activation of mitochondrial pathway and upregulation of DR5 in human lung cancer cells.@*METHODS@#Human non-small-cell lung carcinoma cell lines H460, A549 and H157 were cultured in vitro. The cytotoxic activities were determined using MTT assay. The apoptotic cells death was examined by flow cytometry using PI staining and DNA agarose gel electrophoresis. The activities of caspase-3, -8 and -9 were measured via ELISA. Cellular fractionation was determined by flow cytometry to assess release of cytochrome c and the mitochondrial transmembrane potential. Bcl-2/Bcl-XL/XIAP/Bid/DR5 and DR4 proteins were analyzed using western blot.@*RESULTS@#The concentrations required for a 50% decrease in cell growth (IC(50)) ranged from 1.8 to 3.2 μM. Casticin induced rapid apoptosis and triggered a series of effects associated with apoptosis by way of mitochondrial pathway, including the depolarization of the mitochondrial membrane, release of cytochrome c from mitochondria, activation of procaspase-9 and -3, and increase of DNA fragments. Moreover, the pan caspase inhibitor zVAD-FMK and the caspase-3 inhibitor zDEVD-FMK suppressed casticin-induced apoptosis. In addition, casticin induced XIAP and Bcl-XL down-regulation, Bax upregulation and Bid clearage. In H157 cell line, casticin increased expression of DR5 at protein levels but not affect the expression of DR4. The pretreatment with DR5/Fc chimera protein effectively attenuated casticin-induced apoptosis in H157 cells. No correlation was found between cell sensitivity to casticin and that to p53 status, suggesting that casticin induce a p53-independent apoptosis.@*CONCLUSIONS@#Our results demonstrate that casticin induces caspase-mediated apoptosis via activation of mitochondrial pathway and upregulation of DR5 in human lung cancer cells.