It is a great pleasure for the editor to publish the first special issue of the International Journal of Urology. I am deeply grateful to the authors for their contributions to this special issue.
This special issue contains six Invited Review Articles, three Review Articles, five Editorial Comments, six Original Articles and one Case Report.
This issue entitled “Lower urinary tract dysfunction: from basic science to clinical management” starts with a Foreword by de Groat (Pittsburgh, USA) introducing six Invited Review Articles.
The Review Article by Koike et al. (Tokyo, Japan) discusses the pathophysiology of urinary incontinence in murine models. They highlight stress-induced urinary continence mechanisms mediated by active urethral closure mechanisms, as well as future pharmacological treatments of stress urinary incontinence.
Ishizuka et al. (Matsumoto, Japan) summarize male lower urinary tract (LUT) symptoms and α1D-adrenoceptors. The article reviews research on the α1D-adrenoceptors in the bladder, urethra and prostate focusing on the relationship between expression levels and symptoms of bladder outlet obstruction, and the implications and functional roles of α1D-adrenoceptors subtypes in these organs. The α1D-adrenoceptors in the LUT might play an important role in the pathophysiology of the LUT disorders.
Kapoor et al. (Essex, UK) present an overview of current and prospective treatment strategies of LUT dysfunction in idiopathic Parkinson's disease. Parkinson's disease is characterized by the triad of resting tremor, muscular rigidity and bradykinesia. Often accompanying abnormalities include disorders of equilibrium, posture and autonomic function, including micturition. Symptoms from the lower urinary tract (LUTS) add a significant comorbidity factor in these patients. Various conservative, minimally invasive and surgical treatment options are discussed to prevent harmful sequelae and to improve the quality of life of these patients.
The Original Article by Brandão et al. (Porto, Portugal) focuses on the moment of inertia as a means to evaluate the biomechanical impact of pelvic organ prolapse. They proposed that the moment of inertia can be used as a new parameter to evaluate pelvic floor damage resulting from prolapse.
Hikita et al. (Yonago, Japan) report the clinical outcome of botulinum toxin type A injection into the detrusor muscle for 11 patients with neurogenic detrusor overactivity. Injection of botulinum toxin type A consistently improves bladder control and quality of life.
Fukuta et al. (Sapporo, Japan) summarize the incidence and risk of treatment for benign prostatic hyperplasia (BPH) in their 15-year longitudinal community-based study. They conclude that the severity of LUTS, decreased peak urinary flow rate, enlarged prostate volume, high prostate-specific antigen value and internal prostatic architecture at baseline are independent risk factors for treatment in Japanese males presenting with BPH/LUTS.
Levin et al. (Albany, USA) focus on the duration versus the severity of partial outlet obstruction in rabbits with partial outlet obstruction. They suggest that the etiology for the mechanism of contractile dysfunction is not an oxidative stress.
Song et al. (Seoul, Korea) discuss enhanced angiogenesis and relaxation of the bladder as an early response to bladder outlet obstruction. Cellular remodeling in the bladder secondary to bladder outlet obstruction starts in the early hours, and it includes enhanced angiogenesis and bladder relaxation. Early relief from bladder outlet obstruction is important to preserve bladder structure and function.
Shen et al. (Chongqing, China) describe that platelet-derived growth factor-BB upregulates connexin 43 expression through the activation of extracellular-regulated protein kinase and platelet-derived growth factor receptor-β signaling pathways. They suggest that this signaling pathway might provide a potential target to manipulate detrusor overactivity
The Case Report by Hart et al. (Rochester, USA) describes a patient with steroid-responsive urinary symptoms and an abnormal digital rectal examination that were secondary to immunoglobulin G4-related prostatitis.