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Metastatic castration-resistant prostate cancer (mCRPC) is a progressive stage of prostate cancer that often spreads to the bone. Radium-223, a bone-targeting radiopharmaceutical, has been shown to improve the overall survival in mCRPC in patients without visceral metastasis. However, the impact of prior systemic therapy on the treatment outcome of mCRPC patients receiving radium-223 remains unclear. This study aimed to investigate the optimal choice of systemic therapy before radium-223 in mCRPC patients. The study included 41 mCRPC patients who received radium-223 therapy, with 22 receiving prior enzalutamide and 19 receiving prior abiraterone. The results showed that the median overall survival was significantly longer in the enzalutamide group than in the abiraterone group (25.1 months vs. 14.8 months, p = 0.049). Moreover, the number of patients requiring blood transfusion was higher in the abiraterone group than in the enzalutamide group (9.1% vs. 26.3%, p = 0.16). The study also found that the number of doses of Radium-223 received was significantly associated with overall survival (≥5 vs.

Background Although multiparametric magnetic resonance imaging (mpMRI) is widely used to assess the volume of prostate cancer, it often underestimates the histological tumor boundary. The aim of this study was to evaluate the feasibility of combining prostate health index (PHI) and mpMRI to estimate the histological tumor diameter and determine the safety margin during treatment of prostate cancer. Methods We retrospectively enrolled 72 prostate cancer patients who underwent radical prostatectomy and had received PHI tests and mpMRI before surgery. We compared the discrepancy between histological and radiological tumor diameter stratified by Prostate Imaging-Reporting and Data System (PI-RADS) score, and then assessed the influence of PHI on the discrepancy between low PI-RADS (2 or 3) and high PI-RADS (4 or 5) groups. Results The mean radiological and histological tumor diameters were 1.60 cm and 2.13 cm, respectively. The median discrepancy between radiological and histological tumor diameter of PI-RADS 4 or 5 lesions was significantly greater than that of PI-RADS 2 or 3 lesions (0.50 cm, IQR (0.00–0.90) vs. 0.00 cm, IQR (−0.10–0.20), p = 0.02). In the low PI-RADS group, the upper limit of the discrepancy was 0.2 cm; so the safety margin could be set at 0.1 cm. In the high PI-RADS group, the upper limits of the discrepancy were 1.2, 1.6, and 2.2 cm in men with PHI 60; so the safety margin could be set at 0.6, 0.8, and 1.1 cm, respectively. Conclusions Radiological tumor diameter on mpMRI often underestimated the histological tumor diameter, especially for PI-RADS 4 or 5 lesions. Combining mpMRI and PHI may help to better estimate the histological tumor diameter.

ObjectivesPartial nephrectomy is the standard treatment for the small renal mass. C index, one of the nephrometric systems, was found to be associated with short-term renal functional outcome after laparoscopic partial nephrectomy. We conducted this study to externally validate the application of C index as a prognostic factor of long-term renal functional outcome after open partial nephrectomy (OPN) for small renal mass.Materials and MethodsThe medical records of 65 consecutive patients undergoing OPN from June 2004 to November 2011 were reviewed. C index was calculated on preoperative computed tomography or magnetic resonance images. The estimated glomerular filtration rate was calculated using the modification of diet in renal disease 2 equation. Short-term and long-term renal functional outcomes were assessed by the nadir estimated glomerular filtration rate within postoperative 1 week and 1 to 2 years. The correlation between C index, perioperative parameters, and renal functional outcomes were examined.ResultsThe median C index in our cohort was 2.2. C index was associated with operative time, cold ischemia time, estimated blood loss, and length of hospital stay (p = 0.03, 0.001, 0.001, and 0.02, respectively). On logistic linear regression analysis, C index (p = 0.01) and operative time (p 2.5 (18.1% vs. 0%, p = 0.001).ConclusionC index could serve as an indicator for both short-term and long-term renal functional decrease after OPN. For patients with C index ≤ 2.5, a comprehensive analysis of vascular anatomy and planning for dissection are crucial in preoperative assessment, and every effort should be exerted to minimize renal parenchymal damage during surgery.

Background Nephrologists commonly recommend continuous ambulatory peritoneal dialysis (CAPD) with break-in periods of at least 2 weeks. We investigated the safety and feasibility of shorter break-in periods following surgical implantation of Tenckhoff catheters. Methods We retrospectively examined 310 patients that underwent Tenckhoff catheter implantation for the first time. The early group comprised 226 patients that started CAPD ≤ 14 days after implantation; the late group comprised 84 patients that started CAPD > 14 days after implantation. Catheter-related complications within 6 months were analyzed. Results A total of 310 patients were enrolled. Time to CAPD initiation was shorter in the early group (2.0 ± 2.7 days) than in the late group (40.6 ± 42.8 days) ( p < 0.001). The bridge hemodialysis rate was higher in the late group (57.1%) than in the early group (31.4%) ( p < 0.001). Overall, 33 early-group (14.6%) and 11 late-group patients (13.1%) developed catheter-related complications within 6 months. The early-group complications were leakage ( n = 5), diminished outflow volume ( n = 7), migration ( n = 7), pericatheter hernia ( n = 1), hemoperitoneum ( n = 1), pericatheter infection ( n = 3), and peritonitis ( n = 9). The late-group complications were leakage ( n = 2), diminished outflow volume ( n = 5), migration ( n = 2), and peritonitis ( n = 2). Actuarial freedom from catheter-related complications was similar in both groups (log rank, p = 0.76). Conclusion Early initiation of CAPD with surgically implanted Tenckhoff catheters is feasible and safe. Shorter break-in periods are not associated with more catheter-related complications. The data from our peritoneal dialysis population suggest that early initiation is not associated with an increased number of complications. This needs to be confirmed in a randomized trial.

Solanum lyratum Thunberg (Solanaceae) has been used as a folk medicine for treating liver, lung and esophagus in the Chinese population. Our previous studies have shown that the crude extract of S. lyratum Thunberg (SLE) induced apoptosis in colo 205 human colon adenocarcinoma cells; however, there is no report to show SLE affect immune responses in vivo. In this study, the in vivo effects of SLE on leukemia WEHI-3 cells and immune responses such as phagocytosis and natural killer (NK) cell activity in normal and leukemia mice were investigated. The SLE treatment decreases surface markers of CD3 and Mac-3 in normal and leukemia mice but promoted the cell markers of CD19 and CD11b in normal mice and CD11b in leukemia mice indicating that the precursors of T cells was inhibited and B cells and macrophage were promoted. The SLE treatment promoted the activity of macrophage phagocytosis in the peripheral blood mononuclear cells (PBMC) and peritoneal cells from normal and leukemia mice. The results also showed that NK cells from the normal and leukemia mice after treatment with SLE can kill the YAC-1 target cells. Therefore, the SLE treatment increased macrophage and NK cell activities. These consistent results indicate SLE could be a potent immune responses agent.

Objective: The study was performed to know if the possibility of tumor growth around a stone can be diagnosed immediately following the procedure of endourological surgery.

Aspirin (acetylsalicylic acid) was used to determine the inhibition of arylamine N-acetyltransferase (NAT) activity and DNA adduct formation in a human bladder tumour cell line (T24). The activity of NAT was measured by high-performance liquid chromatography, assaying for the amounts of N-acetyl-2-aminofluorene and N-acetyl-p-aminobenzoic acid and remaining 2-aminofluorene and p-aminobenzoic acid. Two assay systems were used: one with cytosol and the other with intact cells. High-performance liquid chromatography was also used to analyse for the 2-aminofluorene–DNA adducts. Intact bladder tumour cells were used. The results demonstrated that NAT activity and 2-aminofluorene–DNA adduct formation in human bladder tumour cells were inhibited by acetylsalicylic acid in a dose-dependent manner. The effects of acetylsalicylic acid on the values of the apparent Km and Vmax were also determined in both examined systems. The data also indicated that acetylsalicylic acid decreased the apparent values of Km and Vmax from human bladder tumour cells in both cytosol and intact cells. Copyright © 1999 John Wiley & Sons, Ltd.

Treating forgotten indwelling ureteral stents is difficult because forgotten stents become encrusted and fragmented. Therefore, we developed a silk loop with which to loop the lower end of a forgotten ureteral stent during ureterorenoscopy to supply a counterforce, which fixed the stent while separating encrusted stones from the forgotten stent. We evaluated the success of the silk loop method.Nine patients were enrolled in this study from 1997 to 2003. Each patient had a forgotten ureteral stent with renal stones on the tip of the proximal end. All consented to the procedure of silk loop assisted ureterorenoscopic lithotripsy (URSL) with a Lithoclast (Microvasive, Natick, Massachusetts) lithotriptor.We successfully removed the forgotten indwelling stent from all 9 patients with the silk loop assisted URSL method.Silk loop assisted URSL makes the removal of forgotten stents easier. While percutaneous nephrostolithotomy and open surgery produce successful results, the silk loop method is less invasive and expensive, and it minimizes hospital recovery time.

e16139Background: The benefit of adjuvant chemotherapy (AC) for upper tract urothelial cancer (UTUC) is controversial. Pathologic characteristics such as lymphovascular invasion (LVI) and squamous ...

Most of the chemotherapy treatments for bladder cancer aim to kill the cancer cells, but a high recurrence rate after medical treatments is still occurred. Bufalin from the skin and parotid venom glands of toad has been shown to induce apoptotic cell death in many types of cancer cell lines. However, there is no report addressing that bufalin induced cell death in human bladder cancer cells. The purpose of this study was investigated the mechanisms of bufalin-induced apoptosis in a human bladder cancer cell line (T24). We demonstrated the effects of bufalin on the cell growth and apoptosis in T24 cells by using DAPI/TUNEL double staining, a PI exclusion and flow cytometric analysis. The effects of bufalin on the production of reactive oxygen species (ROS), the level of mitochondrial membrane potential (ΔΨ(m)), and DNA content including sub-G1 (apoptosis) in T24 cells were also determined by flow cytometry. Western blot analysis was used to examine the expression of G(0)/G(1) phase-regulated and apoptosis-associated protein levels in bufalin-treated T24 cells. The results indicated that bufalin significantly decreased the percentage of viability, induced the G(0)/G(1) phase arrest and triggered apoptosis in T24 cells. The down-regulation of the protein levels for cyclin D, CDK4, cyclin E, CDK2, phospho-Rb, phospho-AKT and Bcl-2 with the simultaneous up-regulation of the cytochrome c, Apaf-1, AIF, caspase-3, -7 and -9 and Bax protein expressions and caspase activities were observed in T24 cells after bufalin treatment. Based on our results, bufalin induces apoptotic cell death in T24 cells through suppressing AKT activity and anti-apoptotic Bcl-2 protein as well as inducing pro-apoptotic Bax protein. The levels of caspase-3, -7 and -9 are also mediated apoptosis in bufalin-treated T24 cells. Therefore, bufalin might be used as a therapeutic agent for the treatment of human bladder cancer in the future.

Aloe-emodin, one of the anthraquinones, has been shown to have anticancer activity in different kinds of human cancer cell lines. Therefore, the purpose of this study was to investigate the anti-cancer effect of aloe-emodin on human tongue squamous carcinoma SCC-4 cells. The results indicated that aloe-emodin induced cell death through S-phase arrest and apoptosis in a dose- and time-dependent manner. Treatment with 30 microM of aloe-emodin led to S-phase arrest through promoted p53, p21 and p27, but inhibited cyclin A, E, thymidylate synthase and Cdc25A levels. Aloe-emodin promoted the release of apoptosis-inducing factor (AIF), endonuclease G (Endo G), pro-caspase-9 and cytochrome c from the mitochondria via a loss of the mitochondrial membrane potential (DeltaPsi(m)) which was associated with a increase in the ratio of B-cell lymphoma 2-associated X protein (Bax)/B cell lymphoma/leukemia-2 (Bcl-2) and activation of caspase-9 and -3. The free radical scavenger N-acetylcysteine (NAC) and caspase inhibitors markedly blocked aloe-emodin-induced apoptosis. Aloe-emodin thus induced apoptosis in the SCC-4 cells through the Fas/death-receptor, mitochondria and caspase cascade. Aloe-emodin could be a novel chemotherapeutic drug candidate for the treatment of human tongue squamous cancer in the future.

Ampelopsis cantoniensis (AC) has been used as a folk medicine for reducing pain in the Taiwanese population. Our previous studies have shown that the crude extract of AC induced apoptosis in human promyelocytic leukemia HL-60 cells. In this study, the in vivo effects of AC on leukemia WEHI-3 cells and immune responses such as phagocytosis and natural killer (NK) cell activity were investigated. The weights of the livers and spleens were decreased in the AC-treated groups compared to the control groups. The AC treatment increased the percentage of CD3 and CD19 marker cells in WEHI-3-injected mice, indicating that the precursors of T and B cells were inhibited. The AC treatment promoted the activity of macrophage phagocytosis in the peripheral blood mononuclear cells (PBMC) and peritoneal cells. It was found that the NK cells from mice after treatment with AC can kill the YAC-1 target cells. Therefore, the AC treatment increased NK cell activity. In conclusion, AC can affect WEHI-3 cells in vivo and promote macrophage and NK cell activities.

Gynostemma pentaphyllum Makino is known in Asia for its effect on the treatment of hepatitis and cardiovascular diseases. Gypenosides (Gyp) are the major components extracted from Gynostemma pentaphyllum Makino. However, the molecular mechanism underlying the Gyp-induced cell cycle arrest and apoptotic process is unclear. In this study, the chemopreventive role of Gyp in human lung cancer (A549) cells in vitro was evaluated by studying the regulation of the cell cycle and apoptosis. Gyp induced GO/G1 arrest and apoptosis in the human lung cancer A549 cells. Investigation of the cyclin-dependent protein kinase inhibitors by Western blotting showed that p16, p21, p27 and p53 proteins were increased with the increasing time of incubation with Gyp in the A549 cells. This increase may be the major factor by which Gyp caused GO/G1 arrest in the examined cells. Flow cytometric assay and gel electrophoresis of DNA fragmentation also confirmed that Gyp induced apoptosis in the A549 cells. Our data demonstrated that Gyp-induced apoptotic cell death was accompanied by up-regulation of Bax, caspase-3 and caspase-9, but down-regulation of the Bcl-2 levels. Taken together, Gyp appears to exert its anticancer properties by inducing GO/GI-phase arrest and apoptosis via activation of caspase-3 in human lung A549 cancer cells.

Apoptosis is a process that leads to programmed cell death and also a therapeutic target of cancer. In this study, potential apoptotic effects of shikonin on human bladder cancer cells (T24) in vitro were evaluated. Apoptosis induction, cell viability and morphological changes were investigated and caspase-3 and -9 activity was determined by flow cytometric assay and reverse transcription-polymerase chain reaction. The results showed marked differences in G0/G1 cell cycle arrest and cell death of the T24 cells between shikonin treated and untreated groups. Within 72 hours of treatment, shikonin influenced the cyclin dependent kinase (CDK) and cyclin activity by increasing p21 and decreasing cyclin E, CDK2 and CDK4 protein levels. A marked increase was found in apoptosis induction when the T24 cells were treated with shikonin compared to the untreated group, also confirmed by flow cytometry assay. Shikonin also promoted caspase-3 activity, which led to the induction of caspase-activated DNase (CAD) and cleavage poly(ADP-ribose)polymerase. Furthermore, the shikonin-induced apoptosis of the T24 cells was markedly blocked by the broad-spectrum caspase inhibitor, z-VAD-fmk. Shikonin may be a potential agent for the treatment of bladder transitional cell carcinoma since it induces apoptosis through the activation of caspase-3 activity in T24 human bladder cancer cells.

Berberine, an isoquinoline alkaloid, has been shown to possess anticancer properties in some cancer cell lines. Here, we report that in vitro treatment of cervical cancer Ca Ski cells with berberine decreased the percentage of viable Ca Ski cells in a dose-dependent and time-dependent manner. Berberine enhanced the apoptosis of Ca Ski cells with the induction of a higher ratio of p53 and Bax/Bcl-2 proteins, increased levels of reactive oxygen species (ROS) and Ca2+, disruption of the mitochondrial membrane potential, and promotion of caspase-3 activity. In CaSki cells pretreated with the pan-caspase inhibitor zVAD-fmk, the berberine-induced caspase-3 activity and apoptosis were significantly blocked as confirmed by flow cytometric analysis. Western blot also showed that berberine induced the expression of GADD153, a transcription factor involved in apoptosis. Thus berberine increased ROS levels leading to endoplasmic reticulum (ER) stress based on the increase of GADD153 and shown by Ca2+ release from the ER. When the Ca Ski cells were pretreated with catalase, GADD153 production was abrogated and apoptosis was significantly reduced.

The effects of berberine on the in vivo N-acetylation and metabolism of 2-aminofluorene (2-AF) in bladder, blood, colon, kidney, liver, feces and urine samples and brain tissues (cerebrum, cerebellum and pineal gland) of male Sprague-Dawley rats were investigated. Major metabolites, such as 1-OH-2-AAF, 3-OH-2-AAF, 8-OH-2-AAF and 9-OH-2-AAF were found in bladder tissues, 1-OH-2-AAF, 5-OH-2-AAF and 8-OH-2-AAF were found in blood samples, 1-OH-2-AAF, 3-OH-2-AAF, 5-OH-2-AAF, 8-OH-2-AAF and 9-OH-2-AAF were found in colon tissues, 1-OH-2-AAF, 3-OH-2-AAF and 9-OH-2-AAF were found in kidney tissues, 1-OH-2-AAF, 3-OH-2-AAF and 8-OH-2-AAF were found in liver tissues, 1-OH-2-AAF, 3-OH-2-AAF, 5-OH-2-AAF, 7-OH-2-AAF, 8-OH-2-AA and 9-OH-2-AAF were found in feces samples and 1-OH-2-AAF, 3-OH-2-AAF, 5-OH-2-AAF, 7-OH-2-AAF, 8-OH-2-AA and 9-OH-2-AAF were also found in urine samples, 1-OH-2-AAF, 3-OH-2-AAF and 8-OH-2-AAF were found in cerebrum tissues, 1-OH-2-AAF, 3-OH-2-AAF and 7-OH-2-AAF were found in cerebellum tissues. In the control group, however, only 2-AF and 2-AAF were found in pineal gland after rats had been orally treated with 2-AF (50 mg/kg) for 24 h. Pre-treatment of male rats with berberine (40 mg/kg) 24 h prior to the administration of 2-AF (50 mg/kg), as well as the co-administration of berberine and 2-AF led to a decrease in the amounts of 3-OH-2-AAF and an increase in the amounts of 8-OH-2-AAF in bladder tissues. In blood samples, there were significant decreases of 2-AF, 2-AAF, 1-OH-2-AAF and 8-OH-2-AAF, after rats were pre-treated with berberine for 24 h before the addition of 2-AF. However, co-administration of berberine and 2-AF led to an increase in the amounts of 5-OH-2-AAF. In colon tissues, there were significant decreases of 2-AF, 2-AAF, 1-OH-2-AAF and 8-OH-2-AAF in colon samples after rats were treated with berberine for 24 h before the addition of 2-AF. 2-AF, 1-OH-2-AAF, 3-OH-2-AAF and 9-OH-2-AAF levels were significantly different between control and the group treated with berberine and 2-AF at the same time. In kidney tissues, significant decreases of 2-AF and 2-AAF and of 3-OH-2-AAF were observed after rats were treated with both compounds separately and simultaneously. However, 24 h berberine pre-treatment followed by addition of 2-AF led to significant increase of 9-IH-2-AAF. In liver tissues, there were significant decreases of 2-AAF and 1-OH-2-AAF, after co-administration of berberine and 2-AF. The amounts of 2-AAF, 1-OH-2-AAF and 3-OH-2-AAF were significantly different between the control and the group pretreated with berberine 24 h before the addition of 2-AF. In the feces samples, there were significant decreases of 2-AAF, 3-OH-2-AAF, 7-OH-2-AAF, 8-OH-2-AAF and 9-OH-2-AAF after co-administration of berberine and 2-AF. However, the berberine pre-treatment followed by addition of 2-AF led to a significant increase of 2-AF, 2-AAF and 1-OH-2-AAF levels. In urine samples, there were significant differences of 2-AF, 2-AAF, 1-OH-2-AAF, 3-OH-2-AAF, 5-OH-2-AAF, 8-OH-2-AAF and 9-OH-2-AAF after the co-treatment. However, berberine treatment followed by 2-AF led to significant differences in 1-OH-2-AAF and 5-OH-2-AAF levels. In the cerebrum samples, there were significant differences in 1-OH-2-AAF and 8-OH-2-AAF after both berberine co-treatment and pre-treatment. In cerebellum samples, there were also significant differences in the 1-OH-2-AAF and 3-OH-2-AAF levels after both co- and pretreatment. In pineal gland samples, there were significant differences in 2-AAF levels after co-treatment with berberine and 2-AF and 1-OH-2-AAF was also found in both groups. However, berberine pre-treatment followed by 2-AF led to different levels of 2-AF and 2-AAF, but not of 3-OH-2-AAF.

The effects of the gypenosides (Gyp), a component of Gynostemma pentaphyllum Makino, on the cell viability, cell cycle and induction of apoptosis were investigated in human colon cancer colo 205 cells. Gyp was cytotoxic to colo 205 cells with an IC50 of 113.5 microg/ml. The decreasing number of viable cells appeared to be due to the induction of cell cycle arrest and apoptotic cell death, since Gyp induced morphological changes and internucleosomal DNA fragmentation and increased the sub-G1 group. The production of reactive oxygen species and Ca2+ and the depolarization of mitochondrial membrane potential were observed, dose- and time-dependently, after treatment with various concentrations of Gyp. Gyp treatment also gradually decreased the expression of the anti-apoptotic proteins Bcl-2 and Bcl-xl, but increased the expression of the pro-apoptotic protein Bax. Gyp increased the levels of p53 and promoted the release of cytochrome c and the activation of caspase-3 before leading to apoptosis. These results provide information towards an understanding of the mechanisms by which Gyp induces cell cycle arrest and apoptosis in human colon cancer cells.

Introduction: Although many studies have reported that upper urinary tract stones in patients with nonfunctioning kidneys are associated with malignancy, the incidence and frequency of the tumor cell type remain unclear. Therefore, we aimed to investigate the percentage of malignancies present in patients with nonfunctional kidneys who underwent nephrectomy. Materials and Methods: From July 1995 to December 2005, we reviewed a total of 47 patients who underwent nephrectomy to treat a nonfunctional kidney due to urolithiasis with clinical symptoms such as complicated chronic infection. Pathology revealed malignancies in 24 patients. Relationships between clinical presentations and malignancy were analyzed. Results: Malignancy was diagnosed in 24 patients after nephrectomy. Image studies revealed possible malignancy in only 7 patients before surgery. A high incidence (17/24) of transitional cell carcinoma was noted. The remaining malignancies included 5 renal cell carcinomas, 1 squamous cell carcinoma and 1 epidermoid carcinoma. There were 5 deaths during the follow-up interval. Conclusions: There is a high incidence of malignancy associated with nonfunctional kidney caused by stone disease. We suggest careful examination of the pathological specimens from nephrectomy for nonfunctional kidney regardless of clinical manifestations.

It is well known that dietary phenolic compounds can elicit vital cellular responses such as cytotoxicity, cell cycle arrest and apoptosis by activating a cascade of molecular events. Ellagic acid is one of these phenolic compounds, but the exact mechanism of its action is still unclear. The objective of this study was to investigate ellagic acid-induced cell cycle arrest and apoptosis in T24 human bladder cancer cells in vitro. Assays were performed to determine cell viability, cell cycle arrest, apoptosis, caspases-3 activity and gene expression, measured by flow cytometric assay, polymerase chain reaction (PCR) and determination of caspase-3 activity. Ellagic acid significantly reduced the viable cells, induced G0/G1-phase arrest of the cell cycle and apoptosis. Ellagic acid also increased p53 and p21 and decreased CDK2 gene expression, that may lead to the G0/G1 arrest of T24 cells. Ellagic acid also promoted caspase-3 activity after exposure for 1, 3, 6, 12 and 24 h, which led to induction of apoptosis. Furthermore, the ellagic acid-induced apoptosis on T24 cells was blocked by the broad-spectrum caspase inhibitor (z-VAD-fmk).

Objectives To report our experience with hand-assisted laparoscopic nephroureterectomy (HALNU) to treat upper urinary tract transitional cell carcinoma (TCC). In addition, we report the treatment of 4 patients with upper urinary tract TCC and synchronous superficial urinary bladder TCC by HALNU and simultaneous transurethral resection of bladder tumor (TURBT). Methods We retrospectively reviewed 33 patients who had undergone HALNU. Recovery was evaluated according to the Eastern Cooperative Oncology Group performance status. Four patients had concomitant superficial urinary bladder cancer and underwent simultaneous TURBT at the beginning of surgery. We compared our data with those of our open surgery group and previously published data. Results Partial recovery had occurred by 1 week and complete recovery by 4 weeks postoperatively. Conversion to open surgery was required in 2 (6%) of the 33 patients. The complication rate was 24% (8 of 33) without any mortality. The recurrence rate of urinary bladder TCC was 6% (2 of 33). Both patients with recurrent tumor were treated successfully by TURBT and bacille Calmette-Guerin instillation. All 4 patients with synchronous superficial urinary bladder TCC had undergone simultaneous transurethral resection of bladder tumor, and all 4 were disease free at the last follow-up visit. Conclusions Hand-assisted procedures are appropriate for surgeons with limited experience with laparoscopic surgery. In our study, the convalescence of patients was excellent, and the postoperative results were compatible with those of previous studies. To treat upper urinary tract TCC with synchronous urinary bladder TCC, HALNU and TURBT together seems to be a safe and efficient technique.

Arylamine N-acetyltransferase (NAT) plays an important role in the first step of arylamines metabolism. Luteolin has shown antibacterial, antioxidant and antineoplastic activity. To glean insights into the mechanism of action of luteolin, we assessed the effects of luteolin on NAT activity and gene expression and DNA-2-aminofluorene (AF) adduct formation in human bladder cancer T24 cells. By using high performance liquid chromatography, the amounts of N-acetylation of AF and DNA adducts were determined and quantitated. Gene expression was performed by using polymerase chain reaction and gel electrophoresis. The results indicated: 1) luteolin displayed a dose-dependent inhibition of NAT activity and gene expression (NAT1 mRNA) in T24 cells; 2) time-course experiments showed that N-acetylation of AF measured from intact T24 cells was inhibited by luteolin for up to 48 hours; 3) using standard steady-state kinetic analysis, it was demonstrated that luteolin was a possible uncompetitive inhibitor of NAT activity in T24 cells; and 4) the DNA-AF adduct formation in T24 cells was inhibited by luteolin. This report is the first finding which has shown luteolin to affect human T24 cell NAT activity and gene expression (NAT1 mRNA) and DNA-AF adduct formation.

The cytoskeleton plays important roles in cell function and is therefore implicated in the pathogenesis of many human liver diseases, including malignant tumors. The stability of cytokeratin proteins during tumor transformation in human hepatocellular carcinoma has been studied with a molecular approach previously. The results demonstrate that the cytokeratin is modulated in human hepatocellular carcinoma. Besides this, three low molecular weight cytokeratin molecules (named HCC CK) are found.This indicates that these HCC CKs have undergone modulation from the human hepatocyte cytokeratin 18. We also checked the cytokeratin profile of the human hepatoma cell line PLC/PRF/5 with the same methods to ensure the HCC CK molecules are produced by modulation but not protein degradation. The stability of cytokeratin molecules was studied by a different approach. The cytokeratin compositions of human liver cells (Chang cell line) were analysed under the effects of microtubule-disrupting drug (colchicine) by SDS–PAGE, Western blot, immunoprecipitation using a commercially available monoclonal anti-cytokeratin 18 antibody and immunofluorescent staining. Within 1 h of treatment, the microtubule began to collapse and the filamentous structure was shortening. The microtubule had almost collapsed and became fragmented to form a lattice-like network after 24 h of treatment. The cytokeratin was modulated after long-term (24 h) treatment of colchicine, and the molecular weight became 14 kD and the antigenicity was lost. The stability of cytokeratin molecules was related to the intact microtubule network, after disruption of the microtubule the cytokeratin would be modulated. The intact microtubule network was a stabilizing factor of cytokeratin 18 in human liver cells.

A 42-year-old man presented with painful gross hematuria. He appeared acutely ill on physical examination but mentally alert. Vital signs were normal and no abnormal physical findings were found. Urinalysis revealed several red and white blood cells, and film of the kidneys, ureters and bladder detected a bladder stone of about 2.5 cm. (part A of figure). Excretory urography demonstrated hydronephrosis and hydroureter induced by left lower ureteral obstruction. Renal echogram showed moderate hydronephrosis and a thick renal cortex. Cystoscopy revealed mucosa edema (part B of figure) of the right ureteral orifice, and a bladder stone that was suspended by a ureteral fibroepithelial polyp (part C of figure) prolapsed from the left ureteral orifice. The bladder stone was attached by the ureteral fibroepithelial polyp on its lateral side. The stone was fragmented by electrohydraulic lithotripsy using cystoscopy but was incompletely separated from the polyp (part F of figure). Ureteroscopy revealed a ureteral lumen occupied by a fibroepithelial polyp (part D of figure). The polyp was grasped by basket for traction and resected over the root area through the ureteroscope. The base of the polyp was coagulated by an electrode (part E of figure). After cystolithotripsy, cystolitholapaxy and left ureteroscopic polypectomy, a Double-J† internal ureteral stent was inserted (part G of figure). Histological study of the resected specimen indicated an inflamed fibroepithelial polyp.