At 8 weeks after surgery, the CD-augmented tissues contained layered SMA-positive cells, urothelium uroplakin beta-catenin cancer III -positive urothelium, and S100 fibers, similar to normal bladder tissue. The SIS-augmented bladders showed similar results. At 8 weeks after augmentation, the bladder volume of CD-augmented bladders was larger than that at 4 weeks, while the SIS-augmented bladders were the same as those at 4 weeks. The bladder volume of the non-augmented group did not increase. The bladder compliance of the
CD-augmented bladders at 8 weeks was significantly higher than at earlier times. The bladder compliance of neither the non-augmented nor the SIS-augmented groups increased during the study period. Conclusion: Acellular bovine pericardium-derived material could be a suitable biomaterial for bladder augmentations “
“Many theories attempt to explain the complex etiology of overactive bladder syndrome (OAB), but the exact mechanisms of the pathophysiology JNK inhibitor have yet to be fully
understood. Recent findings have suggested that hypercholesterolemia is related with detrusor overactivity (DO), which, in turn, is usually associated with OAB. The present report examines published studies that have associated hypercholesterolemia with DO to determine the grounds on which such studies were based. According to our analysis, OAB and DO are closely related with hypercholesterolemia. Furthermore, DO and OAB may be affected not just by a single factor like hypercholesterolemia, but rather by all components of metabolic syndrome. Several mechanisms, including
autonomic overactivity, artherosclerosis, ischemic change, alteration of nitric oxide synthase (NOS)/NO system and increased Rho-kinase activity may have a role in the relationship between OAB and hypercholesterolemia. Further studies are warranted, however, to evaluate more about the pathophysiology of OAB. Overactive bladder syndrome (OAB) is characterized by an “urgency, with or without urge incontinence, usually with frequency and nocturia”, and detrusor overactivity (DO) is a urodynamic observation characterized by involuntary detrusor contractions during the filling phase and may of be spontaneous or provoked according to the International Continence Society.1 The diagnosis of OAB does not require urodynamic confirmation of DO, although it often is stated that the patient-reported sensation of urinary urgency is the result of a concomitant involuntary detrusor contraction.2 Hence, DO is often, but not invariably, associated with OAB.3 The pathophysiology of OAB is difficult to explain with simply one etiology. Neurologic dysfunction, as well as obstruction-related, congenital, behavioral, age-related, myogenic, ischemic, inflammatory, and many other factors are considered to be causes of OAB.4–6 Likewise, the pathophysiological basis of DO remains incompletely understood.