No abstract

Introduction Over the past 15 years, significant advances have been made in the treatment of erectile dysfunction (ED). The most significant of these advances has been pharmacological treatment of ED with phosphodiesterase type 5 (PDE5) inhibitors. This therapy greatly increased the awareness of ED and has helped stimulate research into the underlying causes of ED. While treatment with PDE5 inhibitors continues to be the current therapy of choice, approximately 40% of men treated with PDE5 inhibitors fail to have significant improvement in erectile function and PDE5 inhibitors do not reverse the vasculopathic processes associated with ED. With this in mind, new therapies must be developed. The treatment with angiogenic growth factors such as vascular endothelial cell growth factor (VEGF) may be one such therapy. Aim This review will focus on defining key terms in the angiogenic process, angiogenic growth factors, and different delivery methods, and summarize results from angiogenic therapies for the treatment of ED. Methods A review of the literature was performed on all angiogenic therapies for the treatment of ED. A brief review on the angiogenic factors was also performed Results Angiogenic therapies for the treatment of ED are possible and promising; however, further investigation is needed to advance clinically. Conclusions Although numerous studies have now employed angiogenic factors for the possible treatment of ED in several animal models, we are still not at the point to begin human investigations. Future studies need to examine proper dosage of the angiogenic agent, route of delivery, time course for delivery, and combination therapies.

Purpose: This review addresses different aspects of testicular torsion from the clinical perspective as well as the basic cellular and molecular events responsible for the post-torsion testicular changes and pathology, including tissue ischemia-reperfusion injury. Materials and Methods: A review of all published literature on testicular torsion was performed by use of two search engines. Results: Testicular torsion, or more correctly termed torsion of the spermatic cord, is a surgical emergency in order to salvage the testis. Its incidence is approximately 1 in 4,000 per annum. Testicular torsion must be treated promptly to avoid loss of the ipsilateral testis; however, even with torsion repair and gross testicular salvage, significant injury may still occur. Conclusions: The cellular and molecular mechanisms leading to ischemiareperfusion injury are incompletely understood, and adjuncts to surgical treatment have received little attention. Understanding the cellular and molecular effects is important because 25% of males with a history of torsion may experience adult infertility. This review emphasizes current knowledge of basic science results and clinical outcomes of testicular torsion.

Introduction Diabetes mellitus (DM) is a major risk factor for developing erectile dysfunction (ED) and men with DM are often less responsive to phosphodiesterase type 5 (PDE5) inhibitors than ED due to other causes. Aims The aim of this study was to explore potential mechanisms whereby PDE5 inhibitors may have reduced efficacy in type 2 DM. Methods At 4 weeks of age, mice were either fed a high-fat diet (HFD) for 22–36 weeks or fed regular chow (control). An additional group of mice in the same genetic background had a genetic form of type 1 DM. Main Outcome Measures Glucose tolerance testing, intracorporal pressures (ICPs), oxidative stress (OS), apoptotic cell death (active caspase-3 and apostain), PDE5, p53, and cyclic guanosine monophosphate (cGMP) levels, and histological examination of inflow arteries were performed in mice fed a HFD and control mice. A group of mice with type 1 DM were studied for PDE5 expression levels. Results All mice fed a HFD had impaired glucose tolerance compared with the age-matched mice fed on standard chow diet (control). HFD fed mice had reduced maximum ICPs following in vivo cavernous nerve electrical stimulation and increased apoptotic cell death, OS, and p53 levels in the corporal tissue. Interestingly, PDE5 levels were increased and cGMP levels were decreased. In contrast, mice with type 1 DM did not have increases in PDE5. Conclusions Taken together, our results suggest that type 2 DM-induced ED is associated with findings that could lead to reduced cGMP and may account for reduced efficacy of PDE5 inhibitors.

Objective: We sought to characterize clinical and pathologic outcomes of advanced mixed germ cell tumors after retroperitoneal lymph node dissection for post-chemotherapy residual masses. Material and methods:Between January 2006 and November 2015, 56 patients underwent retroperitoneal lymph node dissection (RPLND) for residual masses of greater than 1 cm after receiving either primary chemotherapy or salvage chemotherapy. Retrospective review of the patients' characteristics, clinical, pathological, and treatment outcomes were performed after institutional review board (IRB) and ethics committee approval. Results:The mean age at diagnosis was 30 years. Ninety percent of the patients received 3-4 cycles of BEP (bleomycin/etoposide/cisplatin) as primary chemotherapy, and 29% of them salvage chemotherapy prior to lymph node dissection. The mean size of the residual masses after chemotherapy was 6 cm. The histological findings were necrosis in 30%, viable tumor in 34% and teratoma in 36% of the retroperitoneal masses. The mean time to relapse after RPLND was 11 months, out of 9 relapses, 6 were in the retroperitoneum, 1 in the lung and 1 in the kidney and 1 in the contralateral testicle. Conclusion:Our results indicated higher incidence of viable germ cell tumor in the retroperitoneal residual masses after primary and salvage chemotherapy when compared with previously reported global incidence rates.

No abstract

No abstract

No abstract