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Aim To elucidate the precise cellular and molecular mechanisms that underlie urethral fibrogenesis. Methods Endoluminal electrocautery injury (using Karl Storz 10 Fr. Pediatric urethroscope) was employed in male rabbits (n = 6) to create mucosal injury. Retrograde urethrogram (RUG) and endoluminal ultrasound techniques were used to assess severity and changes in luminal cross-sectional area. Six control rabbits were subjected to sham injury, in which the electrocautery was inserted but not powered. Urethral tissues were harvested 30 days postinjury and subjected to RNA sequencing and quantitative polymerase chain reaction (qPCR) to determine changes in gene expression. Histological, immunostaining, and Western blot studies were used to determine changes in protein expression of known markers of fibrosis (eg, collagen, Integrinαv, GIV/Girdin, transforming growth factor-β (TGF-β), and pSMAD1,2,3). Results Trichrome staining confirmed increased connective tissue in urethral scar tissues. Immunostaining revealed a potential role for epithelial to mesenchymal cell transition (EMT) and positive labeling for all fibrotic markers (eg, collagen-1, Integrin αv, GIV/Girdin, transforming growth factor-β (TGF-β), and SMAD1,2,3). Western blot analysis confirmed increased protein levels of these fibrotic markers. Conclusion Our RNA sequencing and qPCR studies, in conjunction with our protein data, suggest that urethral mucosal fibrogenesis may be mediated by novel fibrogenic signaling pathways involving Wnt-β catenin, TGF-β, GIV/Girdin, and EMT which lead to increased collagen deposition. Therapeutic strategies targeting these pathways may be beneficial in attenuating fibrogenesis and stricture progression.

Objectives To estimate the prevalence of fluoroquinolone-resistant rectal flora in patients undergoing transrectal ultrasound-guided prostate needle biopsy and to identify the high-risk groups. Methods From January 2015 to March 2016, rectal swabs of 557 men who underwent transrectal ultrasound-guided prostate needle biopsy were obtained from five institutions. Clinical variables, including demographics, rectal swab culture results and infectious complications, were evaluated. Univariable and multivariable analyses were used to identify the risk factors for fluoroquinolone resistance of rectal flora and infectious complications. Results The incidence of fluoroquinolone-resistant and extended-spectrum beta-lactamase production was 48.1 and 11.8%, respectively. The most common fluoroquinolone-resistant bacteria was Escherichia coli (81% of total fluoroquinolone-resistant bacteria, 39% of total rectal flora), and 16 (2.9%) patients had infectious complications. Univariable and multivariable analysis of clinical parameters affecting fluoroquinolone resistance showed no factor associated with fluoroquinolone resistance of rectal flora. The clinical parameter related to infectious complications after prostate biopsy was a history of operation within 6 months (relative risk 6.60; 95% confidence interval 1.99-21.8, P = 0.002). Conclusions These findings suggest that a risk-based approach by history taking cannot predict antibiotic resistance of rectal flora, and physicians should consider targeted antibiotic prophylaxis or extended antibiotic prophylaxis for Korean patients undergoing transrectal ultrasound-guided prostate biopsy because of high antibiotic resistance of rectal flora.

Objective To investigate the effects of testosterone on cavernosal endothelial progenitor cells (EPCs) in a castrated rat model. Materials and methods In all, 45 male Sprague–Dawley rats (12-weeks old) were divided into control, surgical castration, and castration with testosterone replacement groups. The rats were castrated under ketamine anaesthesia, and testosterone was administered by daily subcutaneous injection of 3 mg/kg testosterone propionate. The corpus cavernosum was obtained after perfusion with 10 mL saline via the abdominal aorta 4 weeks later. The expression of EPC-specific markers [cluster of differentiation 34 (CD34), fetal liver kinase 1 (Flk1), and vascular endothelial (VE)-cadherin] was evaluated by flow cytometry analysis and immunofluorescence staining. Results CD34+/Flk1+ and CD34+/VE-cadherin+ cells were detected in the cavernosal sinusoidal endothelial space. Flow cytometry analysis showed that CD34 and Flk1 double positive cells (EPCs) comprised ≈3.79% of the corpus cavernosum in normal rats. The percentage of EPC marker-positive cells decreased significantly in the castration group (2.8%; P < 0.05) and was restored to 3.56% after testosterone supplementation. Confocal microscopy revealed that the numbers of CD34+/Flk1+ and CD34+/VE-cadherin+ cells decreased in castrated rats compared with controls, but were similar to control levels in rats receiving testosterone replacement. Conclusions The EPC markers were expressed in the cavernosal sinusoidal endothelial space, and the numbers of resident EPCs were regulated by testosterone. These results suggest that testosterone replacement therapy may improve erectile function by modulating EPCs in patients with hypogonadism.

This is a protocol for a Cochrane Review (Intervention). The objectives are as follows: To assess the effects of testosterone compared to placebo or other medical treatments in men with sexual dysfunction.

Objective Patients with lower urinary tract symptoms (LUTS) have a higher prevalence of cardiovascular disease. We evaluated the correlation between LUTS and cardiovascular risk factors in men presenting with benign prostatic hyperplasia (BPH). Methods We retrospectively reviewed the medical records of 295 men with transurethral resection of the prostate for the treatment of BPH and LUTS. Risk factors for cardiovascular disease included: hypertension, diabetes mellitus (DM), smoking, and dyslipidemia. The severity of LUTS measured by the International Prostatic Symptom Score (IPSS), prostate volume, prostate specific antigen (PSA), maximal urinary flow rate (Qmax), and postvoid residual urine (PVR) in subjects with or without cardiovascular risk factors were compared. Results IPSS-total (22.9 ± 7.8 vs. 21.2 ± 7.3, P = 0.01) and obstructive symptom score (13.3 ± 5.2 vs. 11.9 ± 4.7, P = 0.01) was significantly different between men with hypertension and without cardiovascular risk factors. There was no significant difference of variables between subjects with DM, smoking or dyslipidemia and without cardiovascular risk factors. In the Pearson correlation, the systolic and diastolic blood pressure (BP) were related with prostate volume (r = 0.138, P = 0.040; r = 0.163, P = 0.020), IPSS-total (r = 0.139, P = 0.043; r = 0.138, P = 0.043), and an obstructive symptom score (r = 0.168, P = 0.014; r = 0.143, P = 0.037), respectively. Conclusions Men with hypertension are more likely to have a higher IPSS and large prostate volume than men without hypertension. This finding implicates a pathophysiological association between hypertension and LUTS, and the need to manage comorbid symptoms simultaneously.

BMI = body mass indexCT = computed tomographyDVT = deep vein thrombosisEBL = estimated blood lossEERPE = endoscopicextraperitoneal radicalprostatectomyECE = extracapsularextensionEP = extraperitoneal approachGS = Gleason sumHGPIN = high-grade prostaticintraepithelial neoplasiaLN = lymph nodeLRP = laparoscopic radicalprostatectomyMRI = magnetic resonanceimagingNA = not availableOR = odds ratioPCa = prostate cancerPE = pulmonary embolismPLND = pelvic lymph nodedissectionPSA = prostate-specificantigenRARP = robot-assisted radicalprostatectomyRRP = radical retropubicprostatectomySMR = surgical marginpositive rateSVI = seminal vesicleinvasionTP = transperitoneal approach