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Articles by D Wu
Total Records ( 5 ) for D Wu
  P Kirk , M Roughton , J.B Porter , J.M Walker , M.A Tanner , J Patel , D Wu , J Taylor , M.A Westwood , L.J Anderson and D.J. Pennell
 

Background— The goal of this study was to determine the predictive value of cardiac T2* magnetic resonance for heart failure and arrhythmia in thalassemia major.

Methods and Results— We analyzed cardiac and liver T2* magnetic resonance and serum ferritin in 652 thalassemia major patients from 21 UK centers with 1442 magnetic resonance scans. The relative risk for heart failure with cardiac T2* values <10 ms (compared with >10 ms) was 160 (95% confidence interval, 39 to 653). Heart failure occurred in 47% of patients within 1 year of a cardiac T2* <6 ms with a relative risk of 270 (95% confidence interval, 64 to 1129). The area under the receiver-operating characteristic curve for predicting heart failure was significantly greater for cardiac T2* (0.948) than for liver T2* (0.589; P<0.001) or serum ferritin (0.629; P<0.001). Cardiac T2* was <10 ms in 98% of scans in patients who developed heart failure. The relative risk for arrhythmia with cardiac T2* values <20 ms (compared with >20 ms) was 4.6 (95% confidence interval, 2.66 to 7.95). Arrhythmia occurred in 14% of patients within 1 year of a cardiac T2* of <6 ms. The area under the receiver-operating characteristic curve for predicting arrhythmia was significantly greater for cardiac T2* (0.747) than for liver T2* (0.514; P<0.001) or serum ferritin (0.518; P<0.001). The cardiac T2* was <20 ms in 83% of scans in patients who developed arrhythmia.

Conclusions— Cardiac T2* magnetic resonance identifies patients at high risk of heart failure and arrhythmia from myocardial siderosis in thalassemia major and is superior to serum ferritin and liver iron. Using cardiac T2* for the early identification and treatment of patients at risk is a logical means of reducing the high burden of cardiac mortality in myocardial siderosis.

Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT00520559.

  J Li , H Huang , L Sun , M Yang , C Pan , W Chen , D Wu , Z Lin , C Zeng , Y Yao , P Zhang and E. Song
 

Purpose: We aim to examine miR-21 expression in tongue squamous cell carcinomas (TSCC) and correlate it with patient clinical status, and to investigate its contribution to TSCC cell growth, apoptosis, and tumorigenesis.

Experimental Design: MicroRNA profiling was done in 10 cases of TSCC with microarray. MiR-21 overexpression was quantitated with quantitative reverse transcription-PCR in 103 patients, and correlated to the pathoclinical status of the patients. Immunohistochemistry was used to examine the expression of TPM1 and PTEN, and terminal deoxynucleotidyl transferase–mediated dUTP labeling to evaluate apoptosis. Moreover, miR-21 antisense oligonucleotide (ASO) was transfected in SCC-15 and CAL27 cell lines, and tumor cell growth was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, adherent colony formation, and soft agar assay, whereas apoptosis was determined by Annexin V assay, cytochrome c release, and caspase 3 assay. Tumorigenesis was evaluated by xenografting SCC-15 cells in nude mice.

Results: MiR-21 is overexpressed in TSCC relative to adjacent normal tissues. The level of miR-21 is reversely correlated with TPM1 and PTEN expression and apoptosis of cancer cells. Multivariate analysis showed that miR-21 expression is an independent prognostic factor indicating poor survival. Inhibiting miR-21 with ASO in TSCC cell lines reduces survival and anchorage-independent growth, and induces apoptosis in TSCC cell lines. Simultaneous silencing of TPM1 with siRNA only partially recapitulates the effect of miR-21 ASO. Furthermore, repeated injection of miR-21 ASO suppresses tumor formation in nude mice by reducing cell proliferation and inducing apoptosis.

Conclusions: miR-21 is an independent prognostic indicator for TSCC, and may play a role in TSCC development by inhibiting cancer cell apoptosis partly via TPM1 silencing.

  J. J Tomlinson , A Boudreau , D Wu , H. A Salem , A Carrigan , A Gagnon , A. J Mears , A Sorisky , E Atlas and R. J. G. Hache
 

Glucocorticoids are synthesized locally in adipose tissue and contribute to metabolic disease through the facilitation of adipose tissue expansion. Here we report that exposure of human primary preadipocytes to glucocorticoids increases their sensitivity to insulin and enhances their subsequent response to stimuli that promote differentiation. This effect was observed in primary human preadipocytes but not in immortalized 3T3-L1 murine preadipocytes or in fully differentiated primary human adipocytes. Stimulation of insulin signaling was mediated through induction of insulin receptor (IR), IR substrate protein 1 (IRS1), IRS2, and the p85 regulatory subunit of phosphoinositide-3-3-kinase, which led to enhanced insulin-mediated activation of Akt. Although induction of IRS2 was direct, induction of IR and IRS1 by glucocorticoids occurred subsequent to primary induction of the forkhead family transcription factors FoxO1A and FoxO3A. These results reveal a new role for glucocorticoids in preparing preadipocytes for differentiation.

  G Li , A. M Thomas , S. N Hart , X Zhong , D Wu and G. L. Guo
 

As a unique nuclear receptor with only ligand-binding but no DNA-binding domain, small heterodimer partner (SHP) interacts with many transcription factors to inhibit their function. However, the regulation of SHP expression is not well understood. SHP is highly expressed in the liver, and previous studies have shown farnesoid X receptor (FXR) highly induces SHP by binding to a FXR response element (FXRRE) in the promoter of the Nr0b2 gene, which encodes SHP. The FXR-SHP pathway is critical in maintaining bile acid and fatty acid homeostasis. After genome-wide FXR binding by chromatin immunoprecipitation (ChIP) coupled to massively parallel sequencing (ChIP-seq), a novel FXRRE was found in the 3'-enhancer region of the Nr0b2 gene. This downstream inverted repeat separated by one nucleotide is highly conserved throughout mammalian species. We hypothesized that this downstream FXRRE is functional and may mediate a head-to-tail chromatin looping by interacting with the proximal promoter FRXRE to increase SHP transcription efficiency. In the current study, a ChIP-quantitative PCR assay revealed FXR strongly bound to this downstream FXRRE in mouse livers. The downstream FXRRE is important for FXR-mediated transcriptional activation revealed by luciferase gene transcription activation, as well as by deletion and site-directed mutagenesis. The chromatin conformation capture assay was used to detect chromatin looping, and the result confirmed the two FXRREs located in the Nr0b2 promoter and downstream enhancer interacted to form a head-to-tail chromatin loop. To date, the head-to-tail chromatin looping has not been reported in the liver. In conclusion, our results suggest a mechanism by which activation of FXR efficiently induces SHP transcription is through head-to-tail chromatin looping.

  H Chu , M Wang , D Gu , D Wu , Z Zhang , J Tang and Z. Zhang
 

Myeloperoxidase (MPO) is an endogenous oxidant enzyme that generates reactive oxygen species and plays an important role in the aetiology of cancer. The MPO –463G>A polymorphism influences MPO transcription and has been implicated in cancer risk. However, results from published studies on the association between the MPO –463G>A polymorphism and risk of cancer are conflicting. To derive a more precise estimation of association between the MPO –463G>A polymorphism and risk of cancer, we performed a meta-analysis based on 43 case–control studies, including a total of 14 171 cancer cases and 17 319 controls. We used odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength of the association. Overall, individuals with the –463A allele had a 0.93-fold lower cancer risk in a dominant model (OR = 0.93, 95% CI = 0.87–1.00). In the stratified analyses, we observed a similar association in European populations (heterozygote comparison: OR = 0.90, 95% CI = 0.82–0.99) and hospital-based studies (dominant model: OR = 0.88, 95% CI = 0.79–0.99). When stratified by cancer type, however, no significant association was found. The results suggested that the MPO –463A allele does not contribute to the development of cancer. Additional well-designed large studies are required to validate these findings in different populations.

 
 
 
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