ABSTRACT
Objective@#This study aimed to determine the serum Dickkopf 1 (DKK1) levels in ankylosing spondylitis (AS) patients and decipher the mechanism of tumor necrosis factor (TNF)-mediated DKK1 regulation in human AS enthesis cells. @*Methods@#The sera were obtained from 103 patients with AS and 30 healthy controls (HCs). The enthesis of facet joints were obtained from 4 AS patients and 5 controls. The serum levels of DKK1 were measured using ELISA and compared between AS and HCs. The impact of TNF on DKK1 expression in human primary spinal enthesis cells was evaluated using various molecular biology techniques and bone formation indicators. @*Results@#AS patients showed higher serum DKK1 levels than HCs after adjusting for age (917.4 [615.3∼1,310.0] pg/mL vs. 826.2 [670.3∼927.8] pg/mL, p=0.043). TNF treatment promoted bone formation and DKK1 expression in both control enthesis cells and those of AS. This enhanced bone formation by TNF was pronounced in AS-enthesis than those of controls. Mechanically, TNF induced NF-κB activation upregulates the DKK1 transcript level. While, NF-κB inhibitor led to downregulate DKK1 expression in the enthesis. Besides, DKK1 overexpression promoted bone formation in enthesis. @*Conclusion@#TNF induced DKK1 expression in the enthesis through NF-κB activation. TNF-induced DKK1 expression may play a bone formation in the radiologic progression of ankylosing spondylitis.
ABSTRACT
Objective@#This study aimed to determine the serum Dickkopf 1 (DKK1) levels in ankylosing spondylitis (AS) patients and decipher the mechanism of tumor necrosis factor (TNF)-mediated DKK1 regulation in human AS enthesis cells. @*Methods@#The sera were obtained from 103 patients with AS and 30 healthy controls (HCs). The enthesis of facet joints were obtained from 4 AS patients and 5 controls. The serum levels of DKK1 were measured using ELISA and compared between AS and HCs. The impact of TNF on DKK1 expression in human primary spinal enthesis cells was evaluated using various molecular biology techniques and bone formation indicators. @*Results@#AS patients showed higher serum DKK1 levels than HCs after adjusting for age (917.4 [615.3∼1,310.0] pg/mL vs. 826.2 [670.3∼927.8] pg/mL, p=0.043). TNF treatment promoted bone formation and DKK1 expression in both control enthesis cells and those of AS. This enhanced bone formation by TNF was pronounced in AS-enthesis than those of controls. Mechanically, TNF induced NF-κB activation upregulates the DKK1 transcript level. While, NF-κB inhibitor led to downregulate DKK1 expression in the enthesis. Besides, DKK1 overexpression promoted bone formation in enthesis. @*Conclusion@#TNF induced DKK1 expression in the enthesis through NF-κB activation. TNF-induced DKK1 expression may play a bone formation in the radiologic progression of ankylosing spondylitis.
ABSTRACT
Tic disorder is a childhood neuropsychological disorder characterized by abrupt, involuntary, and repetitive stereotyped muscle movement or vocal sound. Tourette's disorder shows a chronic prognosis, and can last for life if no treatment is applied. Although tic disorder has been known for ages, the underlying cause is still not well known. Non-pharmacological treatments have long been used for the tic disorder, but few clinical studies were conducted. However, the European Society for the Study of Tourette's Syndrome recently issued non-pharmacologic guidelines for treatment of tic disorders based on the research findings obtained so far. In addition, guidelines for non-pharmacologic evidence-based treatment were reported in Canada, North America. By synthesizing the newly reported foreign guidelines for treatment and review articles, the aim of this study is to investigate the non-pharmacologic therapies used for treatment of tic disorder or Tourette's disorder.