How Does Chronic Back Pain Influence Quality of Life in Koreans: A Cross-Sectional Study

Study DesignA cross-sectional study.PurposeTo explore the impact of chronic low back pain (CLBP) on individuals' quality of life; to understand current treatment practices and level of satisfaction with treatment in patients with CLBP.Overview of LiteratureAssessing subjective, patient-reported outcomes such as quality of life is essential to health care research.MethodsInfluences of the CLBP were analyzed via a questionnaire, which contained the character of CLBP, effect of pain management, Korean version Oswestry Disability Index (K-ODI) and Korean version of 12-item Short Form Health Survey (SF-12v2).ResultsOf 3,121 subjects who responded, 67.3% had moderate to severe pain; 43.5% presented prolonged CLBP of more than two years; and 32.4% had suffered from sleep disturbance due to pain. 22.8% of the patients were not satisfied with current pain management. The mean K-ODI score was 37.63; and it was positively correlated with the mean pain intensity (r=0.6, p<0.001). The SF-12v2 result was negatively correlated with mean pain intensity (PCS: r=-0.5, p<0.001; MCS: r=-0.4, p<0.001) and also negatively correlated with the K-ODI score (PCS: r=-0.75, p<0.001; MCS: r=-0.5, p<0.001). The conformity between patients and doctors in pain assessment was fair (κ=0.2463).ConclusionsCLBP negatively affects quality of life. Of total 22.8% of the patients were not satisfied with current pain management. Such needs to be taken more seriously by doctors for improvement of satisfaction and quality of life in patients with CLBP

Radiologic Findings of Renal Hemangioma: Report of Three Cases

Renal hemangioma is an uncommon benign tumor which usually causes painless or painful gross hematuria. Its preoperative diagnosis is extremely difficult or even impossible

Cilostazol Prevents Tumor Necrosis Factor-␣-Induced Cell Death by Suppression of Phosphatase and Tensin Homolog Deleted from Chromosome 10 Phosphorylation and Activation of Akt/Cyclic AMP Response Element-Binding Protein Phosphorylation

ABSTRACT This study examines the signaling mechanism by which cilostazol prevents neuronal cell death. Cilostazol (ϳ0.1-100 M) prevented tumor necrosis factor-␣ (TNF-␣)-induced decrease in viability of SK-N-SH and HCN-1A cells, which was antagonized by 1 M iberiotoxin, a maxi-K channel blocker. TNF-␣ did not suppress the viability of the U87-MG cell, a phosphatase and tensin homolog deleted from chromosome 10 (PTEN)-null glioblastoma cell, but it did decrease viability of U87-MG cells transfected with expression vectors for the sense PTEN, and this decrease was also prevented by cilostazol. Cilostazol as well as 1,3-dihydro-1-[2-hydroxy-5-(trifluoromethyl)phenyl]-5-(trifluoromethyl)-2H-benzimidazol-2-one (NS-1619) and (3S)-(ϩ)-(5-chloro-2-methoxyphenyl)-1,3-dihydro-3-fluoro-6-(trifluoromethyl)-2H-indole-2-one (BMS 204352), maxi-K channel openers, prevented increased DNA fragmentation evoked by TNF-␣, which were antagonizable by iberiotoxin. TNF-␣-induced increased PTEN phosphorylation and decreased Akt/ cyclic AMP response element-binding protein (CREB) phosphorylation were significantly prevented by cilostazol, those of which were antagonized by both iberiotoxin and paxilline, maxi-K channel blockers. The same results were evident in U87-MG cells transfected with expression vectors for sense PTEN. Cilostazol increases the K ϩ current in SK-N-SH cells by activating maxi-K channels without affecting the ATP-sensitive K ϩ channel. Thus, our results for the first time provide evidence that cilostazol prevents TNF-␣-induced cell death by suppression of PTEN phosphorylation and activation of Akt/CREB phosphorylation via mediation of the maxi-K channel opening. Recent research has shown that the phosphatase and tensin homolog deleted from chromosome 10 (PTEN) is implicated in the regulation of several cellular functions, including cell viability from apoptosi

Inhibition of HMGB1-induced angiogenesis by cilostazol via SIRT1 activation in synovial fibroblasts from rheumatoid arthritis.

High mobility group box chromosomal protein 1 (HMGB-1) released from injured cells plays an important role in the development of arthritis. This study investigated the anti-angiogenic effects of cilostazol in collagen-induced arthritis (CIA) of mice, and the underlying mechanisms involved. The expressions of HIF-1α, VEGF, NF-κB p65 and SIRT1 in synovial fibroblasts obtained from rheumatoid arthritis (RA) patients were assessed by Western blotting, and in vitro and in vivo angiogenesis were analyzed. Tube formations by human microvascular endothelial cells (HMVECs) were significantly increased by direct exposure to HMGB1 or to conditioned medium derived from HMGB1-stimulated RA fibroblasts, and these increases were attenuated by cilostazol, the latter of which was blocked by sirtinol. HMGB1 increased the expression of HIF-1α and VEGF and concomitantly increased nuclear NF-κB p65 and DNA binding activity, but these effects of HMGB1 were inhibited by cilostazol. SIRT1 protein expression was time-dependently decreased (3-24 hr) by HMGB1, which was recovered by pretreatment with cilostazol (1-30 µM) or resveratrol, accompanying with increased SIRT1 deacetylase activity. In the tibiotarsal joint tissues of CIA mice treated with vehicle, HIF-1α- and VEGF-positive spots and CD31 staining were markedly exaggerated, whereas SIRT1 immunofluorescence was diminished. These variables were wholly reversed in cilostazol (30 mg/kg/day)-treated mice. Furthermore, number of blood vessels stained by von Willebrand factor antibody was significantly lower in cilostazol-treated CIA mice. Summarizing, cilostazol activated SIRT1 and inhibited NF-κB-mediated transcription, thereby suppressing the expression of HIF-1α and VEGF. In addition, cilostazol caused HIF-1α deacetylation by enhancing SIRT1 activity and reduced VEGF production, thereby had an anti-angiogenic effect in vitro studies and in CIA murine model