Similar to other pediatric chronic diseases, nocturnal enuresis is a condition that negatively affects the health related quality of life of children and their mothers. Impaired health related quality of life can be improved after the successful treatment of nocturnal enuresis.
CDK-based risk demonstrated is strongly associated with clinical outcome. CDK-based risk should be an accurate system for predicting recurrence and survival for planning follow-up.
which is induced in the injured liver, was identified as HGF Hepatocyte growth factor activator (HGFA) is a serine activator (HGFA). protease that is responsible for localized activation of HGFA is a serine protease that was purified from bovine hepatocyte growth factor (HGF) in injured tissue. The serum 9 and from human serum. 10 The nucleotide sequence activated HGF may be involved in regeneration of the of the human HGFA complementary DNA (cDNA) revealed injured tissue. HGFA is produced and secreted by the that the mature form of human HGFA purified from serum liver and circulates in the plasma as an inactive zymois derived from the carboxyl deoxycytidine triphosphate-tergen. In response to tissue injury, the HGFA zymogen is minal region of a precursor protein of 655 amino acids and converted to the active form by limited proteolysis. In that the precursor consists of multiple domains homologous this study, we isolated a rat HGFA complementary DNA to those in blood coagulation factor XII. 10 These domains are (cDNA) clone and analyzed the production of HGFA mesa type II fibronectin homology region, two epidermal growth senger RNA (mRNA) in response to tissue injury using factor domains, a type I fibronectin homology region, a krinthis cDNA clone as a probe. The nucleotide sequence of gle domain, and a catalytic domain. HGFA is produced by the cDNA revealed that the amino acid sequences of rat the liver and circulates in plasma as an inactive precursor and human HGFA showed a high degree of conservation (zymogen) form of a serine protease. 11 In response to hepatic in the regions of the characteristic domain structures, injury, the zymogen is activated exclusively in the injured suggesting that rat and human HGFA are activated by liver by limited proteolysis at a specific site. 8 Similarly, in a similar mechanism and have similar enzymatic activiresponse to renal injury, this proteolytic cleavage occurs exties in vivo. Tissue distribution analysis showed that the clusively in the injured kidney. 8 The activated HGFA then liver was the major site of rat HGFA mRNA synthesis.converts inactive HGF to the active form in the injured tisMoreover, the cells producing HGFA mRNA were identisues. fied as parenchymal liver cells. The level of HGFA mRNAAs HGFA is a key enzyme that regulates the activity of increased in the liver after hepatotoxin or nephrotoxin HGF in injured tissues, it is important to characterize HGFA treatment. This increase was also observed during acute production following tissue injury. Thus, we analyzed the inflammation induced by turpentine. These results sugchanges in levels of HGFA messenger RNA (mRNA) in regest that the increase in production of HGFA mRNA in sponse to tissue injury. Most information regarding proteoresponse to tissue injury is the result of an inflammatory lytic activation of HGF and HGFA in injured tissues has been response, and that HGFA is an acute phase protein.obtained in the rat system. 6,8 Therefore, we isolated a cDNA (HEPATOLOGY 1997;25:97-102.)clone encoding rat H...
Introduction Various conservative treatments for Peyronie’s disease (PD) have been attempted over the years. Intralesional verapamil injection has been tested in prospective randomized studies, but the effect of this treatment seems insufficient. Nicardipine is a calcium antagonist alternative to verapamil and is reportedly more effective in vitro. Aim The objective of our study was to evaluate the usefulness of intralesional nicardipine injection as a conservative treatment for PD in the transition period of acute and chronic phase. Methods Eighty-six patients (age: 38–72 years, mean: 52) were enrolled in this study. A total of 74 patients were assigned randomly to nicardipine group (10 mg diluted in 10 mL of distilled water daily, N=37) and control group (10 mL of saline water, N=37). A total of six injections were administrated biweekly. Mean Outcome Measure The subjects were assessed by International Index of Erectile Function (IIEF)-5 and international pain scale. The plaque size was measured by ultrasonography after 20 µg intracavernosal injection of alprostadil (prostaglandin E1). The penile curvature was also measured by taking a photograph at maximum rigidity. Results A reduction of pain score was seen throughout the course of treatment in both groups with a significant difference between the nicardipine and control groups (multiple analysis of variance test, P = 0.019). A significant improvement of IIEF-5 score occurred only in the nicardipine group at 48 weeks after the initiation of treatment (P <0.01). The plaque size was significantly reduced at 48 weeks only in the nicardipine group (12 points, P = 0.0004 by paired t-test). The penile curvature was significantly improved in both groups (P <0.01) without significant difference between them (P = 0.14). There were no severe side effects, such as hypotension or other cardiovascular events. Conclusion Our findings indicate that intralesional nicardipine injection is clinically effective as a conservative treatment for PD in the transition period of acute and chronic phase.
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