Alpha 1-blockers represent the first-line drug treatment of male patients with lower urinary tract symptoms (LUTS), and anticholinergics are often given with alpha 1-blockers because of concerns for developing acute urinary retention. In some patients, however, alpha 1-blockers are ineffective, and in other patients, alpha 1-blockers cannot be continued due to adverse effects. In this open label prospective study, we evaluated the efficacy and safety of solifenacin succinate monotherapy (SOL) in male LUTS patients with overactive bladder (OAB) symptoms, and the influence of prostate volume.

To determine whether ureteroscopic biopsy combined with selective upper-tract cytology can predict muscle invasion in upper urinary tract urothelial carcinoma (UUT-UC) considering radical nephroureterectomy.

Transplantation of mesothelial cells is used to repair peritoneum that is damaged by surgery, peritonitis, and peritoneal dialysis. The largest obstacle for clinical application of mesothelial cell transplantation is the lack of a reliable source of mesothelial cells. So far, they are isolated from omentum, mesentery, parietal wall and ascites. Procedures used to obtain mesothelial cells from the omentum or, mesentery are invasive, however, especially in pre-operative situations. Sufficient amounts of ascites for aspiration can not be obtained under physiological conditions. We have developed a novel method of isolating mesothelial cells from the tunica vaginalis. The tunica vaginalis originates from the peritoneum and descends into the scrotum along with the testis during fetal development. This region provides a source of mesothelial cells that is convenient to approach and free from abdominal complications. Transplantation of autologous mesothelial cells that were isolated from tunica vaginalis was effective in preventing post-operative adhesions. In this review, we summarize mesothelial cell transplantation trials and describe the method of isolating mesothelial cells form the tunica vaginalis. Mesothelial cell transplantation might be widely accepted for clinical. use in the near future.

To determine the significant pathological prognostic factors for upper urinary tract urothelial carcinoma, especially pT3N0M0 stage, and discuss the adequacy for adjuvant chemotherapy.

In the present study, we examined a novel technique to prevent adhesion formation in a rat intestinal hernia model with mesothelial cell sheets cultured on fibrin gel. Mesothelial cells were obtained from isologous rats by enzymatic disaggregation of mesentery and cultured on fibrin gel. Electron microscopy revealed that these cultured cells form contiguous monolayer cell sheets with well-developed microvilli. These tissue-engineered constructs were grafted in vivo to an intestinal hernia model that results in regular surgical adhesions without treatment. Five days postgrafting, rats were sacrificed. Adhesion formation was not observed in rats grafted with the constructs, whereas severe adhesions were observed in all control rats. Constructs seeded with mesothelial cells isolated from EGFP-transgenic rats clearly revealed that grafted mesothelial cells remained at the host tissue site even after fibrin scaffold degradation. These cells developed more abundant microvilli in vivo than those in vitro. These results show that cultured mesothelial cell sheets are effective in preventing adhesion formation and should reduce postoperative complications caused by adhesion formation.

OBJECTIVETo report the development of a new method of isolating autologous mesothelial cells from the tunica vaginalis that are easily obtained and generally free from the effects of abdominal cancer, and to investigate whether transplanting these mesothelial cells is effective in preventing postoperative adhesions.MATERIALS AND METHODSThe tunica vaginalis was resected from male Lewis rats, and mesothelial cells were collected by enzymatic disaggregation. To investigate the efficacy of mesothelial cells in preventing adhesion, harvested cells were transplanted into a rat intestinal hernia adhesion model.RESULTSCells isolated from the tunica vaginalis were homogenous, polygonal when confluent, expressed cytokeratin and vimentin, and the cell surface was covered with microvilli, which is the characteristic appearance of endogenous mesothelial cells. The transplantation of autologous mesothelial cell sheets reduced peritoneal adhesion.CONCLUSIONWe developed a new method of obtaining autologous mesothelial cells from the tunica vaginalis. These cells may provide a valuable option for treating patients at risk of postoperative adhesions.

Metastatic renal cell carcinomas (RCC) remain highly resistant to systemic therapy. RCCs are highly vascular tumors, which overproduce angiogenic peptides such as vascular endothelial growth factor (VEGF) even under normoxic conditions. A potential suggested role of antiangiogenic therapeutic strategies is the treatment of RCC by inhibiting VEGF production. The down-regulation of VEGF expression by glucocorticoids has recently been demonstrated in several cells. In this study, the direct effects of glucocorticoids on VEGF production by RCC cells were evaluated. Four RCC cell lines A498, RCC270, Caki1, and ACHN were treated with dexamethasone (DEX), hydrocortisone (HC), 5-α-dihydrotestosterone (DHT), or estradiol (E2). RU486 was used as a glucocorticoid receptor (GR) antagonist. Cell growth was studied with MTS assays. VEGF mRNA and protein were evaluated with quantitative real-time RT-PCR and ELISA, respectively, and GR expression was examined using RT-PCR and immunocytochemistry. All four RCC cell lines expressed GR. DEX at 100nM down-regulated VEGF secretions by more than 50% in three lines (A498, RCC270, and Caki1) and had a weak inhibitory effect on ACHN cells. The effect of DEX on reducing VEGF mRNA levels in A498 cells was concentration-dependent and maximal at 100nM (80% inhibition). HC had similar but weaker effects on VEGF production in the RCC cells, but E2 and DHT had no effect. RU486 reversed the effects of DEX. DEX at 1–1000nM did not affect cell growth in any of the four RCC cell lines. This is the first study showing that glucocorticoids, at concentrations achievable in vivo by oral administration of low doses of DEX, have an inhibitory effect on VEGF mRNA expression and protein secretion of RCC cells possibly through the GR pathway. Furthermore, DEX might have a potential role in antiangiogenic therapeutic strategies by inhibiting VEGF production during metastatic RCC treatment.

You have accessJournal of UrologyDiscussed Poster, Monday, May 10, 2004, 1:00 - 5:00 pm1 Apr 2004997: Glucocorticoids Down-Regulate Vascular Endothelial Growth Factor (VEGF) Production in Renal Cell Carcinoma Cells Aki Iwai, Yasuhisa Fujii, Satoru Kawakami, Ryoji Takazawa, Yukio Kageyama, and Kazunori Kihara Aki IwaiAki Iwai , Yasuhisa FujiiYasuhisa Fujii , Satoru KawakamiSatoru Kawakami , Ryoji TakazawaRyoji Takazawa , Yukio KageyamaYukio Kageyama , and Kazunori KiharaKazunori Kihara View All Author Informationhttps://doi.org/10.1016/S0022-5347(18)38234-XAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "997: Glucocorticoids Down-Regulate Vascular Endothelial Growth Factor (VEGF) Production in Renal Cell Carcinoma Cells." The Journal of Urology, 171(4S), p. 264 © 2016 by American Urological AssociationFiguresReferencesRelatedDetails Volume 171Issue 4SApril 2004Page: 264 Advertisement Copyright & Permissions© 2016 by American Urological AssociationMetrics Author Information Aki Iwai More articles by this author Yasuhisa Fujii More articles by this author Satoru Kawakami More articles by this author Ryoji Takazawa More articles by this author Yukio Kageyama More articles by this author Kazunori Kihara More articles by this author Expand All Advertisement PDF downloadLoading ...