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Gao L.,University of Newcastle | Gao L.,Deakin University | Xia L.,Renmin University of China | Pan S.-Q.,Renmin University of China | And 2 more authors.
Epilepsy Research | Year: 2015

Objectives: We aimed to gauge the burden of epilepsy in China from a societal perspective by estimating the direct, indirect and intangible costs. Methods: Patients with epilepsy and controls were enrolled from two tertiary hospitals in China. Patients were asked to complete a Cost-of-Illness (COI), Willingness-to-Pay (WTP) questionnaires, two utility elicitation instruments and Mini Mental State Examination (MMSE). Healthy controls only completed WTP questionnaire, and utility instruments. Univariate analyses were performed to investigate the differences in cost on the basis of different variables, while multivariate analysis was undertaken to explore the predictors of cost/cost component. Results: In total, 141 epilepsy patients and 323 healthy controls were recruited. The median total cost, direct cost and indirect cost due to epilepsy were US$949.29, 501.34 and 276.72, respectively. Particularly, cost of anti-epileptic drugs (AEDs) (US$394.53) followed by cost of investigations (US$59.34), cost of inpatient and outpatient care (US$9.62) accounted for the majority of the direct medical costs. While patients' (US$103.77) and caregivers' productivity costs (US$103.77) constituted the major component of indirect cost. The intangible costs in terms of WTP value (US$266.07 vs. 88.22) and utility (EQ-5D, 0.828 vs. 0.923; QWB-SA, 0.657 vs. 0.802) were both substantially higher compared to the healthy subjects. Conclusions: Epilepsy is a cost intensive disease in China. According to the prognostic groups, drug-resistant epilepsy generated the highest total cost whereas patients in seizure remission had the lowest cost. AED is the most costly component of direct medical cost probably due to 83% of patients being treated by new generation of AEDs. © 2014 Elsevier B.V. Source


Gao L.,University of Newcastle | Xia L.,Renmin University of China | Pan S.-Q.,Renmin University of China | Xiong T.,The Fifth Hospital of Wuhan | Li S.-C.,University of Newcastle
Epilepsy and Behavior | Year: 2014

Objectives: This study aimed to translate and validate the Liverpool Seizure Severity Scale (LSSS) in Chinese-speaking patients with epilepsy and explore the determinants of seizure severity in China. Methods: Accepted procedures were followed to translate the LSSS. Each participant was interviewed to complete the LSSS, Seizure Severity Index, Quality of Well-being Scale Self-Administered (QWB-SA), EuroQol (EQ-5D), and Mini Mental State Examination (MMSE). Construct validity and internal consistency were assessed. The determinants of seizure severity were explored. Results: The construct validity of the LSSS was demonstrated by good convergent and discriminant validities. Cronbach's alpha and the intraclass correlation coefficient were 0.886, respectively. In the multivariate analysis, seizure types (p. = 0.001), seizure frequency (p. = 0.001), and numbers of antiepileptic drugs (p. = 0.042) predicted the scores on the LSSS. Types of antiepileptic drugs also contributed to the variation in the LSSS scores. Conclusions: Chinese LSSS is a valid, reliable, and sensitive seizure severity scale. Seizure frequency, seizure types, and quantities and types of AEDs predict seizure severity. © 2013 Elsevier Inc. Source


Ji M.,Renmin University of China | Fan D.,Center Hospital of NayangHenan | Yuan L.,Renmin University of China | Zhang Y.,Renmin University of China | And 2 more authors.
Experimental and Therapeutic Medicine | Year: 2015

Ezrin-radixin-moesin (ERM)-binding phosphoprotein 50 (EBP50) has previously been demonstrated to be associated with the malignant transformation of numerous types of human cancer. The aim of the present study was to investigate the effect of EBP50 overexpression on pancreatic cancer and the underlying mechanism. Reverse transcription-quantitative polymerase chain reaction was used to detect the expression of EBP50 in human pancreatic cancer tissue specimens. Furthermore, pBK-CMV-HA-EBP50 and the pBK-CMV-HA vectors were transfected into pancreatic cancer cells and the effect of EBP50 upregulation on the proliferation and invasion of the cells was investigated. In addition, the effect of EBP50 overexpression on β-catenin and E-cadherin expression was evaluated. The results revealed that overexpression of EBP50 suppressed cell growth and invasion in two human pancreatic cancer cell lines. Overexpression of EBP50 also suppressed β-catenin expression and increased E-cadherin expression. Thus, the present study demonstrated that EBP50 inhibits pancreatic cancer cell growth and invasion through targeting the β-catenin/E-cadherin pathway. The results suggest that EBP50 may function as a potential tumor suppressor and thus may serve as a potential therapeutic target. © 2015 Spandidos Publications. All rights reserved. Source


Ji M.,Renmin University of China | Yuan L.,Criminal Science and Technology Studio | Lv X.,Renmin University of China | Dong W.,Renmin University of China | Peng X.,The Fifth Hospital of Wuhan
Experimental and Therapeutic Medicine | Year: 2014

Increasing evidence has demonstrated that ezrin-radixin-moesin (ERM)-binding phosphoprotein 50 (EBP50) is involved in the malignant transformation of numerous human cancers. The present study investigated the involvement of EBP50 overexpression in the tumorigenicity of pancreatic cancer (PC). The results revealed that overexpression of EBP50 suppressed cell growth, promoted cell apoptosis and arrested G1-to-S phase progression in two human PC cell lines. Overexpression of EBP50 also suppressed B-cell lymphoma 2 (Bcl-2) expression. Furthermore, nude mouse tumor xenograft models were established by the subcutaneous injection of cell lines stably transfected with an EBP50-expressing plasmid. The in vivo data indicated that overexpression of EBP50 inhibited the growth of the PC tumors and induced cell apoptosis. Thus, the present study demonstrated that EBP50 overexpression induces growth inhibition and apoptosis in PC by decreasing Bcl-2 expression. The results suggest that EBP50 may function as a potential tumor suppressor in vivo and in vitro. Source


Xiang W.,Huazhong University of Science and Technology | He J.,Huazhong University of Science and Technology | Huang C.,Huazhong University of Science and Technology | Chen L.,Huazhong University of Science and Technology | And 7 more authors.
Oncotarget | Year: 2015

Inactivation of human SET domain containing protein 2 (SETD2) is a common event in clear cell renal cell carcinoma (ccRCC). However, the mechanism underlying loss of SETD2 function, particularly the post-transcriptional regulatory mechanism, still remains unclear. In the present study, we found that SETD2 was downregulated and inversely correlated with high expression of miR-106b-5p in ccRCC tissues and cell lines. Over-expression of miR-106b-5p resulted in the decreased mRNA and protein levels of SETD2 in ccRCC cells. In an SETD2 3'-UTR luciferase reporter system, miR-106b-5p downregulated the luciferase activity, and the effects were abolished by mutating the predicted miR-106b-5p binding site. Moreover, attenuation of miR-106b-5p induced cell cycle arrest at G0/G1 phase, suppressed cell proliferation, enhanced processing of caspase-3, and promoted cell apoptosis in ccRCC cells, whereas these effects were reversed upon knockdown of SETD2. In addition, transfection of miR-106b-5p antagomir resulted in the increased binding of H3K36me3 to the promoter of p53 and enhanced its activity, as well as upregulated the mRNA and protein levels of p53, and the effects were also abolished by cotransfection with si-SETD2. Collectively, our findings extend the knowledge about the regulation of SETD2 at the posttranscriptional level by miRNA and regulatory mechanism downstream of SETD2 in ccRCC. Source

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