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Articles by W Yu
Total Records ( 3 ) for W Yu
  W Yu , M Cline , L. G Maxwell , D Berrigan , G Rodriguez , A Warri and L. Hilakivi Clarke
 

The possibility that dietary vitamin D3 (VD3) exposure inhibits endometrial carcinogenesis in an animal model and modifies the enhanced risk of endometrial carcinoma associated with obesity was investigated. At 4 weeks of age, Pten+/– and wild-type mice were each divided into four treatment groups and fed AIN93G control diet, or AIN93G-based diet containing either 25,000 international units of VD3 per kilogram of diet, 58% fat to induce obesity (high fat), or high fat and 25,000 international units of VD3 per kilogram of diet. Mice were kept on these diets until they were sacrificed at week 28. Although VD3 did not affect endometrial cancer risk, it inhibited obesity-induced increase in endometrial lesions. Specifically, high-fat diet increased focal glandular hyperplasia with atypia and malignant lesions from 58% in the control diet–fed Pten+/– mice to 78% in obese mice. Dietary VD3 decreased the incidence of endometrial pathology in obese Pten+/– mice to 25% (P < 0.001). VD3 altered the endometrial expression of 25-hydroxylase, 1-hydroxylase, and vitamin D receptor in the wild-type and Pten+/– mice. Estrogen receptor- mRNA levels were higher (P < 0.014) and progesterone receptor protein levels in the luminal epithelium were lower (P < 0.04) in the endometrium of control diet–fed Pten+/– than wild-type mice, but the expression of these receptors was not affected by the dietary exposures. VD3 reversed the obesity-induced increase in osteopontin (P < 0.001) and significantly increased E-cadherin expression (P < 0.019) in the endometrium of obese Pten+/– mice. Our data confirm the known association between obesity and endometrial cancer risk. Dietary exposure to VD3 inhibited the carcinogenic effect of obesity on the endometrium. This protective effect was linked to a reduction in the expression of osteopontin and increase in E-cadherin. Cancer Prev Res; 3(10); 1246–58. ©2010 AACR.

  A. S Barth , T Aiba , V Halperin , D DiSilvestre , K Chakir , C Colantuoni , R. S Tunin , V. L Dimaano , W Yu , T. P Abraham , D. A Kass and G. F. Tomaselli
 

Background— Cardiac electromechanical dyssynchrony causes regional disparities in workload, oxygen consumption, and myocardial perfusion within the left ventricle. We hypothesized that such dyssynchrony also induces region-specific alterations in the myocardial transcriptome that are corrected by cardiac resynchronization therapy (CRT).

Methods and Results— Adult dogs underwent left bundle branch ablation and right atrial pacing at 200 bpm for either 6 weeks (dyssynchronous heart failure, n=12) or 3 weeks, followed by 3 weeks of resynchronization by biventricular pacing at the same pacing rate (CRT, n=10). Control animals without left bundle branch block were not paced (n=13). At 6 weeks, RNA was isolated from the anterior and lateral left ventricular (LV) walls and hybridized onto canine-specific 44K microarrays. Echocardiographically, CRT led to a significant decrease in the dyssynchrony index, while dyssynchronous heart failure and CRT animals had a comparable degree of LV dysfunction. In dyssynchronous heart failure, changes in gene expression were primarily observed in the anterior LV, resulting in increased regional heterogeneity of gene expression within the LV. Dyssynchrony-induced expression changes in 1050 transcripts were reversed by CRT to levels of nonpaced hearts (false discovery rate <5%). CRT remodeled transcripts with metabolic and cell signaling function and greatly reduced regional heterogeneity of gene expression as compared with dyssynchronous heart failure.

Conclusions— Our results demonstrate a profound effect of electromechanical dyssynchrony on the regional cardiac transcriptome, causing gene expression changes primarily in the anterior LV wall. CRT corrected the alterations in gene expression in the anterior wall, supporting a global effect of biventricular pacing on the ventricular transcriptome that extends beyond the pacing site in the lateral wall.

  L Zhang , J Chen , Y Wang , F Ren , W Yu and L. Cheng
  BACKGROUND

Levonorgestrel (LNG), as a dedicated emergency contraception (EC) product, has been available over-the-counter in China for 10 years. Until now, only a small number of deliveries after LNG–EC failure have been documented.

METHODS

This study was a prospective comparative cohort study. A group of 332 pregnant women who had used LNG–EC during the conception cycle was recruited, and matched to a group of 332 pregnant women without the exposure to LNG. Congenital malformations, perinatal complications and delivery circumstances were investigated in this study.

RESULTS

There were 31 pregnant women in the study group and 28 in the comparison group miscarried within 14 weeks of gestation. In the study and comparison groups, four malformations were found in each group. In the study group, both birthweight (3416 versus 3345 g, P = 0.040) and the sex ratio of birth (boys/girls, 1.14 versus 0.90, P = 0.153) were higher than in the comparison group. There were no statistically significant differences in the incidence of miscarriage or malformation or in the neonatal outcome between the two groups.

CONCLUSIONS

There was no association between the use of LNG–EC pills and the risk of major congenital malformations, pregnancy complications or any other adverse pregnancy outcomes in our study.

 
 
 
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