Conclusion: Treatment of OAB
with solifenacin is associated with significant improvement in generic HRQoL and disease-specific symptoms at 8 weeks after drug administration. DNA Damage inhibitor Particularly for generic HRQoL as measured by the SF-36, solifenacin treatment effectively improves three SF-36 scores: PF, VT, and MH. “
“Objectives: It has been reported that nitric oxide (NO) mainly contributes to prostate or urethral smooth muscles relaxation, and that nitrergic innervation and neuronal NO synthase (nNOS) levels are decreased in benign prostatic hyperplasia. The purpose of the present study was to evaluate the feasibility to gene therapy for benign prostatic hyperplasia by transferring nNOS gene into the rat prostate with in vivo electroporation (EP) procedure. Methods: Male Sprague–Dawley rats were divided
into four groups (sham, only EP, only nNOS injection, and nNOS gene injection with EP groups). Fifty micrograms of luciferase gene and nNOS expression vectors in 50 µL of K-PBS (potassium-phosphate buffered saline) were injected into the prostate. Immediately after the injection of these vectors, the vector injection points were electroporated by the two-square parallel https://www.selleckchem.com/EGFR(HER).html electrodes. Two days after gene transfer, luciferase analysis and an immunohistochemical staining for nNOS were performed, and NO2−/NO3− (NOX) release was measured using high-performance liquid chromatography coupled with the
microdialysis procedure. Results: The optimal electric pulse conditions were 50 V, 1 Hz and 10 msec. In vivo EP with these conditions showed the increase in the luciferase gene expression approximately 300-fold of the control group. In the nNOS gene injection with EP group, the marked nNOS immunoreactivity was observed, and NOX release was significantly higher, as compared to other groups. Conclusion: The results suggest that EP is a feasible technique for in vivo gene transfer into the rat prostate, and that the transferred nNOS gene functionally expresses and contributes to NO production. “
“Bladder hypertrophy and dysfunction are well-known bladder responses to outlet obstruction (i.e. urodynamic overload). Cardiac hypertrophy and heart failure are also caused by hemodynamic overload, and Staurosporine many basic and clinical studies suggest that the local renin-angiotensin system (RAS) has a crucial role in load-induced cardiac pathogenesis. The similarity of the response of the heart and the bladder to overload suggests that angiotensin II (AngII) may have a similar regulatory role in pathological remodeling, such as muscle growth and collagen production of the obstructed bladder. Previous in vitro studies show that angiotensin I is converted to AngII by angiotensin converting enzyme (ACE) or chymase, which exists in the human bladder.
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