Management of nocturnal enuresis in Taiwan: Consensus statements of the Taiwan enuresis expert committee.

Nocturnal enuresis causes significant psychological distress to affected children and their family and requires appropriate management. A 12-member expert committee of pediatric urologists and pediatric nephrologists in Taiwan with extensive experience in treating enuresis was established to develop consensus statements and a recommended treatment algorithm for the management of patients with nocturnal enuresis in Taiwan after careful consideration of current evidence, existing guidelines, and expert opinion as well as local practice and culture. The finalized consensus statements were reviewed by and have received endorsement from the Taiwan Urological Association and the Taiwan Pediatric Association. Patients with suspected enuresis should undergo a thorough initial assessment to fully evaluate urinary signs and symptoms and to rule out underlying causes of diurnal and nocturnal incontinence. Behavioral therapy is recommended throughout the course of management. Desmopressin in the fast-melting formulation is the recommended first-line pharmacological treatment. Combination therapy may be effective in patients who have failed first-line treatment. These consensus statements and a recommended treatment algorithm were created by the expert committee to provide practical support for clinical decision making by physicians in Taiwan.

Prostate Health Index (PHI) improves prostate cancer detection at initial biopsy in Taiwanese men with PSA 4-10 ng/mL.

In this study, we aimed to validate the Prostate Health Index (PHI) for the detection of prostate cancer (PCa). We prospectively enrolled patients aged 50-75 years with a serum prostate specific antigen (PSA) level of 4-10 ng/mL undergoing transrectal biopsy of the prostate between April 2016 and May 2017. The primary outcome was the diagnostic performance of various PSA derivatives (total PSA, free PSA, %fPSA, p2PSA, %p2PSA, and PHI) to predict PCa. The secondary outcome was comparisons of PSA derivatives between patients with a Gleason score (GS) ≤6 and GS ≥7. PCa was diagnosed in 36 of 154 (23.4%) patients, and 26 (16.9%) had a GS ≥7. The areas under the receiver operating characteristic curves were significantly greater in %p 2PSA and PHI than in PSA (0.76 vs. 0.57, p = 0.015 and 0.77 vs. 0.57, p = 0.004, respectively). Patients with a GS ≥7PCa had marginally higher %p2PSA and PHI than those with a GS of 6 (17.8 vs. 12.73, p = 0.06; 46.58 vs. 31.55, p = 0.05). At a PHI cutoff value of 29.6, the sensitivity and specificity were 77.8% and 67.8% in detecting PCa, respectively. In addition, 57.1% of the patients avoided an unnecessary biopsy, while three patients (1.9%) with GS 7 PCa were missed. In conclusion, the ability of %p2PSA and PHI to predict prostate biopsy outcome was better than that of PSA and %fPSA in the initial biopsy in Taiwanese men with serum PSA between 4 and 10 ng/mL.

Lotus leaf (Nelumbo nucifera) and its active constituents prevent inflammatory responses in macrophages via JNK/NF-κB signaling pathway.

Inflammation is a serious health issue worldwide that induces many diseases, such as inflammatory bowel disease (IBD), sepsis, acute pancreatitis and lung injury. Thus, there is a great deal of interest in new methods of limiting inflammation. In this study, we investigated the leaves of Nelumbo nucifera Gaertn, an aquatic perennial plant cultivated in eastern Asia and India, in anti-inflammatory pharmacological effects in the murine macrophage cell line RAW264.7. Results showed that lipopolysaccharide (LPS) increased the protein expression of inducible nitric oxide synthase (iNOS) and COX-2, as well as the mRNA expression and level of IL-6 and TNF-α, while NNE significantly reduced these effects of LPS. LPS also induced phospho-JNK protein expression. The JNK-specific inhibitor SP600125 decreased the proteins expression of phospho-JNK, iNOS, COX-2, and the mRNAs expression and levels of IL-6 and TNF-α. Further, NNE reduced the protein expression of phospho-JNK. LPS was also found to promote the translocation of NF-κB from the cytosol to the nucleus and to decrease the expression of cytosolic IκB. NNE and SP600125 treatment recovered the LPS-induced expression of NF-κB and IκB. While phospho-ERK and phospho-p38 induced by LPS, could not be reversed by NNE. To further investigate the major components of NNE in anti-inflammatory effects, we determined the quercetin and catechin in inflammatory signals. Results showed that quercetin and catechin significantly decreased the proteins expression of iNOS, COX-2 and phospho-JNK. Besides, the mRNAs and levels of IL-6 and TNF-α also decreased by quercetin and catechin treatment in LPS-induced RAW264.7 cells. These results showed that NNE and its major components quercetin and catechin exhibit anti-inflammatory activities by inhibiting the JNK- and NF-κB-regulated pathways and could therefore be an useful anti-inflammatory agent.

Spontaneous ureteral rupture and review of the literature.

INTRODUCTION: Spontaneous ureteral rupture is defined as non-traumatic urinary leakage from the ureter. This is a diagnosis that, although uncommon, is important for emergency physicians to know about. The literature is relatively sparse. MATERIALS AND METHODS: This was a retrospective review of patients who were diagnosed with spontaneous ureteral rupture. From 2006 to 2012, 18 patients were diagnosed by radiography (computed tomography or intravenous urogram) with spontaneous ureteral rupture. These cases all showed extravasation of the contrast outside the excretory system. We evaluated underlying causes, diagnostic and therapeutic procedures, and outcomes. RESULTS: There were 9 men and 9 women with a median age of 59 years (range, 22-82 years). In 56% of patients, a ureteral stone was the cause; in 17% of, a ureteral stricture; in 1 patient, a ureteral tumor; and in the remaining 22%, no cause was identified. In 13 patients (72.2%), primary ureteroscopy to place D-J stents was performed. The average duration of ureteral catheter stenting was 21 days (range, 8-45 days). The other 5 patients (27.8%) were managed conservatively with antibiotic treatment and the outcome was good. CONCLUSIONS: Ureteral stones most commonly cause spontaneous ureteral rupture. In our experience, most patients received ureteroscopy and Double-J stenting. Conservative management with antibiotics also had good outcomes. Most patients had sudden onset of abdominal or flank pain. Spontaneous ureteral rupture should be kept in the differential diagnosis of patients with acute abdominal or flank pain in the emergency department.

Arsenic induces reactive oxygen species-caused neuronal cell apoptosis through JNK/ERK-mediated mitochondria-dependent and GRP 78/CHOP-regulated pathways.

Arsenic (As), a well-known high toxic metal, is an important environmental and industrial contaminant, and it induces oxidative stress, which causes many adverse health effects and diseases in humans, particularly in inorganic As (iAs) more harmful than organic As. Recently, epidemiological studies have suggested a possible relationship between iAs exposure and neurodegenerative disease development. However, the toxicological effects and underlying mechanisms of iAs-induced neuronal cell injuries are mostly unknown. The present study demonstrated that iAs significantly decreased cell viability and induced apoptosis in Neuro-2a cells. iAs also increased oxidative stress damage (production of malondialdehyde (MDA) and ROS, and reduction of Nrf2 and thioredoxin protein expression) and induced several features of mitochondria-dependent apoptotic signals, including: mitochondrial dysfunction, the activations of PARP and caspase cascades, and the increase in caspase-3 activity. Pretreatment with the antioxidant N-acetylcysteine (NAC) effectively reversed these iAs-induced responses. iAs also increased the phosphorylation of JNK and ERK1/2, but did not that p38-MAPK, in treated Neuro-2a cells. NAC and the specific JNK inhibitor (SP600125) and ERK1/2 inhibitor (PD98059) abrogated iAs-induced cell cytotoxicity, caspase-3/-7 activity, and JNK and ERK1/2 activation. Additionally, exposure of Neuro-2a cells to iAs triggered endoplasmic reticulum (ER) stress identified through several key molecules (GRP 78, CHOP, XBP-1, and caspase-12), which was prevented by NAC. Transfection with GRP 78- and CHOP-specific si-RNA dramatically suppressed GRP 78 and CHOP expression, respectively, and attenuated the activations of caspase-12, -7, and -3 in iAs-exposed cells. Therefore, these results indicate that iAs induces ROS causing neuronal cell death via both JNK/ERK-mediated mitochondria-dependent and GRP 78/CHOP-triggered apoptosis pathways.

Cadmium induces apoptosis in pancreatic ß-cells through a mitochondria-dependent pathway: the role of oxidative stress-mediated c-Jun N-terminal kinase activation.

Cadmium (Cd), one of well-known highly toxic environmental and industrial pollutants, causes a number of adverse health effects and diseases in humans. The growing epidemiological studies have suggested a possible link between Cd exposure and diabetes mellitus (DM). However, the toxicological effects and underlying mechanisms of Cd-induced pancreatic ß-cell injury are still unknown. In this study, we found that Cd significantly decreased cell viability, and increased sub-G1 hypodiploid cells and annexin V-Cy3 binding in pancreatic ß-cell-derived RIN-m5F cells. Cd also increased intracellular reactive oxygen species (ROS) generation and malondialdehyde (MDA) production and induced mitochondrial dysfunction (the loss of mitochondrial membrane potential (MMP) and the increase of cytosolic cytochrome c release), the decreased Bcl-2 expression, increased p53 expression, poly (ADP-ribose) polymerase (PARP) cleavage, and caspase cascades, which accompanied with intracellular Cd accumulation. Pretreatment with the antioxidant N-acetylcysteine (NAC) effectively reversed these Cd-induced events. Furthermore, exposure to Cd induced the phosphorylations of c-jun N-terminal kinases (JNK), extracellular signal-regulated kinases (ERK)1/2, and p38-mitogen-activated protein kinase (MAPK), which was prevented by NAC. Additionally, the specific JNK inhibitor SP600125 or JNK-specific small interference RNA (si-RNA) transfection suppressed Cd-induced ß-cell apoptosis and related signals, but not ERK1/2 and p38-MAPK inhibitors (PD98059 and SB203580) did not. However, the JNK inhibitor or JNK-specific si-RNA did not suppress ROS generation in Cd-treated cells. These results indicate that Cd induces pancreatic ß-cell death via an oxidative stress downstream-mediated JNK activation-triggered mitochondria-regulated apoptotic pathway.

Chloroacetic acid induced neuronal cells death through oxidative stress-mediated p38-MAPK activation pathway regulated mitochondria-dependent apoptotic signals.

Chloroacetic acid (CA), a toxic chlorinated analog of acetic acid, is widely used in chemical industries as an herbicide, detergent, and disinfectant, and chemical intermediates that are formed during the synthesis of various products. In addition, CA has been found as a by-product of chlorination disinfection of drinking water. However, there is little known about neurotoxic injuries of CA on the mammalian, the toxic effects and molecular mechanisms of CA-induced neuronal cell injury are mostly unknown. In this study, we examined the cytotoxicity of CA on cultured Neuro-2a cells and investigated the possible mechanisms of CA-induced neurotoxicity. Treatment of Neuro-2a cells with CA significantly reduced the number of viable cells (in a dose-dependent manner with a range from 0.1 to 3mM), increased the generation of ROS, and reduced the intracellular levels of glutathione depletion. CA also increased the number of sub-G1 hypodiploid cells; increased mitochondrial dysfunction (loss of MMP, cytochrome c release, and accompanied by Bcl-2 and Mcl-1 down-regulation and Bax up-regulation), and activated the caspase cascades activations, which displayed features of mitochondria-dependent apoptosis pathway. These CA-induced apoptosis-related signals were markedly prevented by the antioxidant N-acetylcysteine (NAC). Moreover, CA activated the JNK and p38-MAPK pathways, but did not that ERK1/2 pathway, in treated Neuro-2a cells. Pretreatment with NAC and specific p38-MAPK inhibitor (SB203580), but not JNK inhibitor (SP600125) effectively abrogated the phosphorylation of p38-MAPK and attenuated the apoptotic signals (including: decrease in cytotoxicity, caspase-3/-7 activation, the cytosolic cytochrome c release, and the reversed alteration of Bcl-2 and Bax mRNA) in CA-treated Neuro-2a cells. Taken together, these data suggest that oxidative stress-induced p38-MAPK activated pathway-regulated mitochondria-dependent apoptosis plays an important role in CA-caused neuronal cell death.

Mercuric compounds induce pancreatic islets dysfunction and apoptosis in vivo.

Mercury is a toxic heavy metal that is an environmental and industrial pollutant throughout the world. Mercury exposure leads to many physiopathological injuries in mammals. However, the precise toxicological effects of mercury on pancreatic islets in vivo are still unclear. Here, we investigated whether mercuric compounds can induce dysfunction and damage in the pancreatic islets of mice, as well as the possible mechanisms involved in this process. Mice were treated with methyl mercuric chloride (MeHgCl, 2 mg/kg) and mercuric chloride (HgCl(2), 5 mg/kg) for more than 2 consecutive weeks. Our results showed that the blood glucose levels increased and plasma insulin secretions decreased in the mice as a consequence of their exposure. A significant number of TUNEL-positive cells were revealed in the islets of mice that were treated with mercury for 2 consecutive weeks, which was accompanied by changes in the expression of the mRNA of anti-apoptotic (Bcl-2, Mcl-1, and Mdm-2) and apoptotic (p53, caspase-3, and caspase-7) genes. Moreover, plasma malondialdehyde (MDA) levels increased significantly in the mice after treatment with mercuric compounds for 2 consecutive weeks, and the generation of reactive oxygen species (ROS) in the pancreatic islets also markedly increased. In addition, the mRNA expression of genes related to antioxidation, including Nrf2, GPx, and NQO1, were also significantly reduced in these islets. These results indicate that oxidative stress injuries that are induced by mercuric compounds can cause pancreatic islets dysfunction and apoptosis in vivo.

Paraquat induces lung alveolar epithelial cell apoptosis via Nrf-2-regulated mitochondrial dysfunction and ER stress.

Paraquat (1,1'-dimethyl-4,4'-bipyridinium chloride; PQ) is widely and commonly used as a herbicides in the world. PQ has been reported to be a major hazard because it causes lung injury. However, the molecular mechanisms underlying PQ-induced lung toxicity still need to be elucidated. Here, we found that PQ significantly decreases cell viability, increases sub-G1 hypodiploids DNA contents and caspase 3/7 activity in lung alveolar epithelial cell-derived L2 cells, which also caused mitochondrial dysfunction, and decreased the mRNA expression of Bcl-2 and increased that of Bax, Bak, and p53. Moreover, the protein expressions of Bax and Bak were increased in PQ-treated cells. In addition, when PQ was exposed to L2 cells, the expressions of ER stress-related signaling genes (including Grp78, CHOP, and caspase-12 mRNA) and proteins (including phospho-eIF-2α, CHOP, Grp78, calpain I and -II, and caspase-12) were significantly increased. PQ also decreased the protein expressions of pro-caspase-9/7/3. Next, we investigated the role of Nrf-2 in PQ-induced alveolar epithelial cell toxicity. In L2 cells, PQ induced Nrf-2 translocation from the cytosol to the nucleus. Cells transfected with Nrf-2 siRNA significantly reversed the PQ-induced toxicity, including depolarization of MMP, increased the Bax, Bak, p53 mRNAs expression, decreased the Bcl-2 mRNA expression, increased the caspase 3/7 activity, Grp78, CHOP, and caspase-12 mRNAs and protein expression, and decreased that of pro-caspase-3. Taken together, these results suggest that Nrf-2-regulated mitochondria and ER stress-related pathways are involved in the PQ-induced alveolar epithelial cell injury.

The impact of gender and size on the pathology of small renal mass.

Without surgery, it is hard to predict the histology of small (≦ 4 cm) renal masses (SRMs) based on images. This study attempted to investigate whether clinical parameters were correlated with the pathological presence of SRM carcinomas. We conducted a retrospective chart review of 60 patients with 61 suspicious SRMs on radiological examination who received radical nephrectomy (RN) or partial nephrectomy (PN) between January 2003 and February 2011 in the China Medical University Hospital (CMUH). The correlations between patient age, gender, tumor size, and pathological features were calculated and analyzed. Of the 61 SRMs, there were 51 (83.6%) renal cell carcinoma (RCC), seven (11.5%) angiomyolipoma, two (3.3%) oncocytoma, and one (1.6%) metanephric adenoma. Regarding the histological variants of these cases of RCC, 44 were categorized as the clear cell type, two as the papillary type, and five as the chromophobe type. The incidence of benign tumor was greater in females (p=0.014) and tumor size 2 cm or less (p=0.02), compared with males and tumor size more than 2 cm, respectively. Surgical intervention is generally recommended for medically fit patients.

Involvement of oxidative stress-induced ERK/JNK activation in the Cu(2+)/pyrrolidine dithiocarbamate complex-triggered mitochondria-regulated apoptosis in pancreatic ß-cells.

Oxidative stress was demonstrated to promote the progression of diabetes mellitus (DM). It has been suggested that copper may play a specific role in the progression and pathogenesis of DM. Pyrrolidine dithiocarbamate (PDTC), a widely apply to the medicine, was known to be capable of enhancing copper accumulation. In this study, we investigated the effect of submicromolar-concentration Cu(2+)/PDTC complex on pancreatic ß-cell damage and evaluated the role of oxidative stress in this effect. CuCl(2) (0.01-300µM) did not affect the cell viability in ß-cell line RIN-m5F cells. However, combination of CuCl(2) (0.5µM) and PDTC (0.3µM) markedly reduced RIN-m5F cell viability. Cu(2+)/PDTC complex could also increase the LPO and decrease the intracellular reduced GSH levels, and display several features of apoptosis signals including: increase in sub-G1 cell population, annexin-V binding, and caspase-3 activity, mitochondrial dysfunctions, and the activation of PARP and caspase cascades, which accompanied with the marked increase the intracellular Cu(2+) levels. These apoptotic-related responses of Cu(2+)/PDTC complex-induced could be effectively prevented by antioxidant N-acetylcysteine (NAC). Furthermore, Cu(2+)/PDTC complex was capable of increasing the phosphorylations of ERK1/2 and JNK, and its upstream kinase MEK1/2 and MKK4, which could be reversed by NAC. Transfection with ERK2- and JNK-specific si-RNA and specific inhibitors SP600125 and PD98059 could inhibit ERK1/2 and JNK activation and attenuate MMP loss and caspase-3 activity induced by the Cu(2+)/PDTC complex. Taken together, these results are the first report to demonstrate that the Cu(2+)/PDTC complex triggers a mitochondria-regulated apoptosis via an oxidative stress-induced ERK/JNK activation-related pathway in pancreatic ß-cells.

Nickel(II) induced JNK activation-regulated mitochondria-dependent apoptotic pathway leading to cultured rat pancreatic ß-cell death.

Nickel (Ni), a well-known toxic metal, is widely used in electroplating and alloy production. It is also significantly implicated in industrial and environmental pollution caused by uncontrolled industrial and municipal discharges. In this study, we characterized and investigated the cytotoxic effects of Ni exposure and their probable toxicological mechanisms in the pancreatic ß-cells. The results showed that it was significantly decreased cell viability after exposing pancreatic ß-cell-derived RIN-m5F cells to NiCl(2) for 24h in a dose-dependent manner. NiCl(2) also increased sub-G1 hypodiploid cells and Annexin V-Cy3 binding population in RIN-m5F cells, indicating that it has apoptosis-inducing ability. Moreover, the exposure of RIN-m5F cells to NiCl(2) induced distinct signals of mitochondria-dependent apoptosis, including mitochondrial dysfunction (the disruption of mitochondrial membrane potential (MMP) and increase in mitochondrial cytochrome c release into the cytosol), Bak and Bid mRNA up-regulation, and activation of caspase-3, caspase-7, and caspase-9, and poly(ADP-ribose) polymerase (PARP) degradation. In addition, NiCl(2) also markedly induced the activation of c-Jun N-terminal kinases (JNK), but not of extracellular signal-regulated kinase (ERK)1/2 and p38. These NiCl(2)-induced apoptosis-related signaling responses could be effectively reversed by specific JNK inhibitor SP600125. To the best of our knowledge, this study is the first to show that Ni causes pancreatic ß-cell death through a JNK activation-regulated mitochondria-dependent apoptosis-signaling pathway.

Involvement of oxidative stress-mediated ERK1/2 and p38 activation regulated mitochondria-dependent apoptotic signals in methylmercury-induced neuronal cell injury.

Methylmercury (MeHg) is well-known for causing irreversible damage in the central nervous system as well as a risk factor for inducing neuronal degeneration. However, the molecular mechanisms of MeHg-induced neurotoxicity remain unclear. Here, we investigated the effects and possible mechanisms of MeHg in the mouse cerebrum (in vivo) and in cultured Neuro-2a cells (in vitro). In vivo study showed that the levels of LPO in the plasma and cerebral cortex significantly increased after administration of MeHg (50µg/kg/day) for 7 consecutive weeks. MeHg could also decrease glutathione level and increase the expressions of caspase-3, -7, and -9, accompanied by Bcl-2 down-regulation and up-regulation of Bax, Bak, and p53. Moreover, treatment of Neuro-2a cells with MeHg significantly reduced cell viability, increased oxidative stress damage, and induced several features of mitochondria-dependent apoptotic signals, including increased sub-G1 hypodiploids, mitochondrial dysfunctions, and the activation of PARP, and caspase cascades. These MeHg-induced apoptotic-related signals could be remarkably reversed by antioxidant NAC. MeHg also increased the phosphorylation of ERK1/2 and p38, but not JNK. Pharmacological inhibitors NAC, PD98059, and SB203580 attenuated MeHg-induced cytotoxicity, ERK1/2 and p38 activation, MMP loss, and caspase-3 activation in Neuro-2a cells. Taken together, these results suggest that the signals of ROS-mediated ERK1/2 and p38 activation regulated mitochondria-dependent apoptotic pathways that are involved in MeHg-induced neurotoxicity.

Pyrrolidine dithiocarbamate (PDTC)/Cu complex induces lung epithelial cell apoptosis through mitochondria and ER-stress pathways.

Pyrrolidine dithiocarbamate (PDTC) is widely used in pesticides, fungicides, insecticides, and herbicides. Copper (Cu) is a toxic heavy metal in the environment, and an essential trace metal element in the body, which is involved in many biological processes as a catalytic cofactor. The present study is designed to investigate the cellular toxicity of PDTC, CuCl(2), and PDTC/Cu complex exposure in lung alveolar epithelial cells that serve primary structural and functional roles in the lungs. The results showed that PDTC or CuCl(2) alone did not affect cell viability, but PDTC/Cu complex significantly decreased lung alveolar epithelial cell viability. PDTC/Cu complex also significantly increased intracellular copper concentration, but PDTC or CuCl(2) alone had low levels of copper. PDTC/Cu complex dramatically enhanced the JNK protein phosphorylation and ERK protein phosphorylation proteins. PDTC/Cu complex did not affect the p38 protein phosphorylation. PDTC/Cu complex was capable of activating the apoptosis-related caspases including caspase-9, caspase-7, and caspase-3, which could be reversed by the addition of JNK inhibitor SP600125 or transfection of MAPK8 short hairpin RNA. PDTC/Cu complex also increased cytosolic cytochrome c and decreased mitochondrial transmembrane potential. The Bcl-2 mRNA and protein expressions were decreased in lung epithelial cells treated with PDTC/Cu complex, which could be reversed by SP600125. Furthermore, PDTC/Cu complex could trigger the expressions of ER stress-associated signaling molecules including Grp78, Grp94, caspase-12, ATF4, and CHOP, which could be reversed by SP600125. Taken together, these results indicate that exposure to PDTC/Cu complex induces cytotoxicity and apoptosis in alveolar epithelial cells via the mitochondria- and ER-stress-related signaling pathways.

Women urinate in the standing position do not increase post-void residual urine volumes.

AIMS: The effects of standing while voiding have seldom been investigated in women. We evaluate urodynamic parameters of voiding while standing in healthy women using uroflowmetry and post-void residual urine volume assessment. Results are compared with crouching and sitting. METHODS: Between July and October, 2008, a total of 30 healthy, nulliparous female volunteers were enrolled. Ages were 22-37 (mean: 28±4). Urodynamic studies were performed for all in sitting, crouching and standing positions; 3, 3 and 5 times in each position, respectively. Volunteers used homemade auxiliary appliances for collecting urine from the urethra and draining it forward when standing. Volume, maximum flow rate, mean flow rate and post-void residual urine volume were compared. RESULTS: Maximum and average flow rates in the sitting and standing positions were significantly different, but not between sitting and crouching or between crouching and standing. There were no differences in voided volume and post-void residual urine volume. There's no apparent learning curve for women in the standing position. CONCLUSIONS: Though flow rates are decreased while standing, post-void residual volume is not significantly different. Women have another choice for voiding in public restrooms.

Salvage penile curvature correction surgery.

It is commonly believed that coarser suture materials should be used to provide sufficient tenacity in surgery for penile curvature correction. We report our 15-year experience of fine sutures in a second operation in 31 patients who underwent prior curvature correction elsewhere with coarser sutures, resulting in recurrent penile curvature. Suture materials used in prior surgeries in these patients were either 2-0 or 3-0 nylon sutures. In this series, all 31 patients underwent a modified Nesbit procedure at the level of the collagen bundles using finer sutures. Prior to July 1998, 10 men underwent salvage surgery using 4-0 polyglactin sutures. Thereafter, we adapted 6-0 nylon sutures for another 21 patients. We categorized the patients into the polyglactin (n = 10) and nylon (n = 21) groups respectively. Overall, 29 patients were available for follow-up while using the abridged 5-item version of the International Index of Erectile Function (IIEF-5) scoring system, with 21 patients in the nylon group. We have found cavernosography a practical and reliable method to objectively assess penile morphology in these patients. The penile morphology both subjectively and objectively was excellent in all patients, except for 1 in each group. Erectile function restoration showed a trend of satisfaction in the polyglactin group and based on IIEF-5 was significantly improved in the nylon group (14.2 ± 3.6 vs 21.9 ± 2.1, n = 20, P < .001). These results suggest that in penile tunical surgery, fine sutures such as 6-0 nylon may result in better penile morphology and functional outcomes.

Clinical experience of a refined penile venous stripping surgery procedure for patients with erectile dysfunction: is it a viable option?

Penile venous surgery might not be considered an appropriate treatment for erectile dysfunction (ED) because of disappointing functional outcomes and unacceptable, seemly unavoidable, penile deformity. We report results of a refined penile venous stripping method in patients with veno-occlusive dysfunction (VOD). From 2000 to 2003, 341 of 467 men with ED were diagnosed with VOD via cavernosography and Doppler sonography. Patients were excluded from undertaking cavernosography if they had an untreated chronic systemic disease. Patients who had undergone the first penile venous surgery in other institutes were also excluded from this study because of the protracted surgical time and unpredictable functional outcomes, because severe fibrosis may prevent patients from completing penile venous removal. Of these 341 men, 178 were treated with a refined venous stripping surgical method (surgery group) and 163 patients were treated without this surgery (control group). In the surgery group, 167 were available for long-term follow-up using the abridged 5-item version of the International Index of Erectile Function (IIEF-5) scoring system. The operative time ranged from 2.1 to 5.0 hours. The follow-up period ranged from 5.1 to 8.2 years, with an average of 7.7 +/- 1.4 years. The difference between the preoperative (9.7 +/- 3.9) and postoperative (21.6 +/- 2.8) IIEF-5 scores was significant (P < .001). Overall, 90.4% of the surgery group (151 of 167) reported improvements after surgery. A significant decrease in IIEF-5 scores (10.4 +/- 3.8 vs 7.9 +/- 3.2, P < .001, n = 121) during the same period of follow-up was, however, noted in the control group. This refined penile venous stripping surgery delivered favorable results and is a viable alternative for treating VOD.

Salvaging penile venous stripping surgery.

Disappointing functional outcome and penile deformity are major concerns of penile venous surgery. Consequently, it has been abandoned by most urologists. To explore whether penile deformity is correctable and erectile function can be improved, we report our experience in patients who had undergone surgery elsewhere. From 1986 to 2008, 16 consecutive patients sought our assistance because of poorer erectile capability or/and penile deformity from previous venous surgery elsewhere. The abridged 5-item version of the International Index of Erectile Function (IIEF-5) was used to score the patients when it became available in 1998. Accordingly, 3 and 13 patients were categorized into the non-IIEF and IIEF groups, respectively. A median longitudinal pubic incision and a circumferential or semicircumcision were made to relieve the fibrotic tissues for accessing the deep dorsal veins, which were stripped thoroughly and ligated with 6-0 nylon sutures. The cavernosal veins were managed in a similar manner. The paraarterial veins were ligated only segmentally. Finally, the wound was approximated while an assistant consistently stretched the penile shaft. The operation time was 5.2 to 8.5 hours. The follow-up period ranged from 0.6 to 23.0 years. Overall, all patients reported satisfactory penile morphology postoperatively. In the IIEF group, the difference in preoperative and postoperative scores was significant (P < .001). In the non-IIEF group, 2 of the 3 patients reported natural coitus. This series of salvaging venous surgeries, although technically challenging, are helpful in correcting penile deformity and restoring erectile function in some patients who had poorer outcomes from prior venous surgeries.

Bioengineered corporal tissue for structural and functional restoration of the penis.

Various reconstructive procedures have been attempted to restore a cosmetically acceptable phallus that would allow normal reproductive, sexual, and urinary function in patients requiring penile reconstruction. However, these procedures are limited by a shortage of native penile tissue. We previously demonstrated that a short segment of the penile corporal body can be replaced using naturally derived collagen matrices with autologous cells. In the current study, we examined the feasibility of engineering the entire pendular penile corporal bodies in a rabbit model. Neocorpora were engineered from cavernosal collagen matrices seeded with autologous cells using a multistep static/dynamic procedure, and these were implanted to replace the excised corpora. The bioengineered corpora demonstrated structural and functional parameters similar to native tissue and male rabbits receiving the bilateral implants were able to successfully impregnate females. This study demonstrates that neocorpora can be engineered for total pendular penile corporal body replacement. This technology has considerable potential for patients requiring penile reconstruction.