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This article has been retracted at the request of the Editor. The authors have plagiarized part of a paper where the data has been taken from another group of scientists. Readers can find the original Mingzhi Shen's Ph.D thesis, written in Chinese language, Role of Thioredoxin-interacting protein (TXNIP)-Wnt in diabetic myocardial infarction-induced angiogenetic suppression which is included in CNKI (China National Knowledge Infrastructure), http://cdmd.cnki.com.cn/Article/CDMD-90032-1014047242.htm. One of the conditions of submission of a paper for publication is that authors declare explicitly that their work is original and has not appeared in a publication elsewhere. Re-use of any data should be appropriately cited. As such this article represents a severe abuse of the scientific publishing system. The scientific community takes a very strong view on this matter and apologies are offered to readers of the journal that this was not detected during the submission process.
ABSTRACT
Objective: To explore the regulatory role of thioredoxin-interacting protein (TXNIP) in Wnt/β-catenin signaling pathway and therefore to elucidate its function in diabetic myocardial infarction. Methods: Diabetic myocardial infarction models were generated in mice. The expression levels of TXNIP and β-catenin and level of reactive oxygen species (ROS) were determined and compared with those in control group. Human umbilical vein endothelial cells were treated with high-concentration glucose and/or silencing TXNIP and/or H
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<p><b>BACKGROUND</b>Permanent atrial fibrillation (AF) is the most common form of dysrhythmia associated with atrial septal defects (ASDs) in patients older than 40 years. However, little is known about cardiac remodeling after transcatheter closure in patients with permanent AF. This study was designed to compare cardiac events and remodeling effects after transcatheter closure in such patients.</p><p><b>METHODS</b>Clinical data of 289 adult patients older than 40 years who underwent ASD closure at our center were analyzed retrospectively. Of them, 63 patients with permanent AF were assigned to the case group, and the other 226 patients without permanent AF were assigned to the control group. Cardiac events and changes in left and right cardiac cavity dimensions before the procedure and 6 months after the procedure were compared between the two groups.</p><p><b>RESULTS</b>Patients in the case group were significantly older than those in the control group. The right ventricular (RV) volume and right atrial (RA) volume were decreased significantly in both the groups during a median follow-up period of 6 months after closure (P < 0.001). The left atrial dimensions, left ventricular end-systolic dimensions, left ventricular end-diastolic dimensions and left ventricular ejection fraction showed no significant change before and after the procedure in both the groups. Changes of the RV volume and RA volume in the case group were significantly smaller than those in the control group (P = 0.005 and P < 0.001). The New York Heart Association cardiac function was improved in both the groups during the 6 months follow-up period.</p><p><b>CONCLUSIONS</b>The transcatheter closure of ASD can improve the cardiac remodeling and cardiac function in patients with or without AF.</p>
Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Atrial Fibrillation , Therapeutics , Cardiac Catheterization , Methods , Heart Septal Defects, Atrial , Therapeutics , Retrospective StudiesABSTRACT
OBJECTIVE@#To explore the regulatory role of thioredoxin-interacting protein (TXNIP) in Wnt/β-catenin signaling pathway and therefore to elucidate its function in diabetic myocardial infarction.@*METHODS@#Diabetic myocardial infarction models were generated in mice. The expression levels of TXNIP and β-catenin and level of reactive oxygen species (ROS) were determined and compared with those in control group. Human umbilical vein endothelial cells were treated with high-concentration glucose and/or silencing TXNIP and/or H2O2. After 24 h, expression levels of TXNIP, β-catenin and its downstream protein Cyclin D1, and C-myc gene were determined by real-time PCR, Western blot and immunofluorescence method. The cell proliferation and ROS production capability in different groups were determined by methyl thiazolyl tetrazolium assay.@*RESULTS@#Compared with control group, hyperglycemia significantly up-regulated TXNIP expression and ROS level in the myocardium and endothelial cells of myocardial infarction area, whereas the β-catenin expression was down-regulated, and the difference was statistically significant (P < 0.05). In comparison with Human umbilical vein endothelial cells in the control group, high glucose level increased the levels of TXNIP expression and ROS level in cells, but reduced cell proliferation as well as migration capability and expression levels of β-catenin, Cyclin D1 and C-myc; the difference was statistically significant (P < 0.05). However, this trend can be partially reversed by silencing TXNIP.@*CONCLUSIONS@#Diabetic myocardial ischemia could up-regulate levels of TXNIP expression and ROS production in endothelial cells of myocardial infarction area. The regulation effect of TXNIP on β-catenin was partially achieved by changing ROS levels.