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Zeng Q.,Chinese PLA General Hospital | Yuan Y.,Chinese Institute of Aviation Medicine | Wang S.,Chinese PLA General Hospital | Sun J.,Chinese PLA General Hospital | And 2 more authors.
Canadian Journal of Cardiology | Year: 2013

Background: Genome-wide association studies have identified 2 single-nucleotide polymorphisms (SNPs) on chromosome arm 9p21, rs10757278, and rs2383207 that confer susceptibility to myocardial infarction. However, these data are mostly from Italian, American Caucasian, South Korean, and Japanese cohorts. This study is the firstto investigate whether 6 SNPs (rs10757277, rs10757278, rs10757279, rs1333049, rs1333047, and rs10811656) are associated with acute coronary syndrome (ACS) in a Chinese Han population. Methods: We performed a case-control analysis in 359 patients with ACS diagnosed by coronary angiography and 398 non-ACS controls of Han background between April 2007 and January 2008 to determine whether these 6 SNPs were associated with ACS. Exon fragments were genotyped by polymerase chain reaction-restriction fragment length polymorphism. Results: After we adjusted for clinical parameters, we found the rs10757278 GG genotype to be associated with a significantly elevated risk of ACS (odds ratio [OR], 1.91; 95% confidence interval [CI], 1.35-2.68; P= 0.00035), the rs10811656 T allele to be associated with a higher risk of ACS (OR, 1.67; 95% CI, 1.26-2.23; P= 0.0016) than the CC genotype, and the rs1333047 TT genotype also to be associated with a higher risk of ACS (OR, 1.57; 95% CI, 1.15-2.06; P= 0.0052) than the CC and CT genotypes. After 14.2 ± 4.5 months of follow-up, the end-point data were obtained: death (cardiac and noncardiac), nonfatal myocardial infarction, and recurrent angina leading to repeated coronary angiography. We found that the rs10757278 GG genotype was significantly associated with recurrent angina compared with the AA and AG genotypes (P= 0.013). Conclusions: Polymorphisms on 9p21 were associated with ACS in a Chinese Han population. The rs10757278 GG genotype was further associated with adverse cardiac outcomes after ACS. © 2013 Canadian Cardiovascular Society. Source


Chen D.,Zhejiang University | Zhang A.,Shanghai JiaoTong University | Fang M.,Shaoxing Women and Childrens Hospital | Fang R.,Huzhou Maternity and Child Care Hospital | And 8 more authors.
BMC medical genetics | Year: 2014

BACKGROUND: Offspring of pregnancy complicated with gestational diabetes (GDM) are at high risk for metabolic diseases. The mechanisms behind the association of intrauterine exposure to GDM and high risk of health problems in later life remain largely unknown. The aim of this study was to clarify the alteration in methylation levels at differentially methylated regions (DMRs) of GNAS and IGF2 in fetuses of GDM women and to explore the possible mechanisms linking maternal GDM with high risk of metabolic diseases in later life of GDM offspring.METHODS: Lymphocytes were isolated from umbilical cord blood of infants born to 87 women with GDM and 81 women with normal pregnancy. Genomic DNA was extracted and DNA methylation levels of GNAS and IGF2 DMRs were determined by Massarray quantitative methylation analysis.RESULTS: The methylation levels were detected in 7 CpG sites of GNAS DMRs and 6 sites of IGF2 DMRs. Methylation levels were significantly higher at sites 4, 5 and 7 of GNAS DMR in GDM compared to normal pregnancy (P = 0.007, 0.008 and 0.008, respectively). The methylation level at site 4 of GNAS was significantly correlated with the presence of GDM (P = 0.003), the methylation levels at site 5 and 7 were significantly correlated with the presence of GDM (P = 0.002 for both) and gestational age (P = 0.027 for both). There was no significant difference in any sites of IGF2 DMR (P > 0.05 for all).CONCLUSIONS: We concluded maternal GDM-induced hypermethylation at GNAS DMR and this condition may be among the mechanisms associating maternal GDM with increased risk of metabolic diseases in later life of offspring. Source


He J.,Zhejiang University | Zhang A.,Shanghai JiaoTong University | Fang M.,Shaoxing Women and Childrens Hospital | Fang R.,Huzhou Maternity and Child Care Hospital | And 9 more authors.
BMC Genomics | Year: 2013

Background: Offspring of pregnancy complicated with preeclampsia are at high risk for hypertension, stroke and possibly obesity. The mechanisms behind the association of intrauterine exposure to preeclampsia and high risk of health problems in the later life remain largely unknown. The aims of the current investigation were to determine the changes in DNA methylation at IGF2 and GNAS DMR in offspring of preeclamptic pregnancy and to explore the possible mechanisms underlying the association between maternal preeclampsia and high risk for health problems in the later life of their offspring.Results: Umbilical cord blood was taken from infants born to women of preeclampsia (n=56), gestational hypertension (n=23) and normal pregnancy (n=81). DNA methylation levels of IGF2 and GNAS DMR were determined by Massarray quantitative methylation analysis. Methylation levels at IGF2 DMR were significantly lower in preeclampsia than normal pregnancy. The average methylation level at IGF2 DMR was significantly correlated with preeclampsia even after birth weight, maternal age, gestational age at delivery and fetal gender were adjusted. The difference in methylation level was not significantly different between mild and severe preeclampsia. The methylation level at GNAS DMR was not significantly correlated with birth weight, maternal age, gestational age at delivery, fetal gender, preeclampsia or gestational hypertension.Conclusions: We concluded preeclampsia induced a decrease in methylation level at IGF 2 DMR, and this might be among the mechanisms behind the association between intrauterine exposure to preeclampsia and high risk for metabolic diseases in the later life of the infants. © 2013 He et al.; licensee BioMed Central Ltd. Source


Xie Z.-P.,Shaoxing Women and Childrens Hospital | Zhao B.-W.,Zhejiang University | Yuan H.,Shaoxing Women and Childrens Hospital | Hua Q.-Q.,Shaoxing Women and Childrens Hospital | And 6 more authors.
International Journal of Fertility and Sterility | Year: 2013

Background: To establish the reference range of the angle between ascending aorta and main pulmonary artery of fetus in the second and third trimester using spatiotemporal image correlation (STIC), and to investigate the value of this angle in prenatal screening of conotruncal defects (CTDs). Materials and Methods: Volume images of 311 normal fetuses along with 20 fetuses with congenital heart diseases were recruited in this cross-sectional study. An offline analysis of acquired volume datasets was carried out with multiplanar mode. The angle between aorta and pulmonary artery was measured by navigating the pivot point and rotating axes and the reference range was established. The images of ascending aorta and main pulmonary artery in fetuses with congenital heart diseases were observed by rotating the axes within the normal angle reference range. Results: The angle between ascending aorta and main pulmonary artery of the normal fetus (range: 59.1°~97.0°, mean ± SD: 78.0° ± 9.7°) was negatively correlated with gestational age (r = -0.52; p<0.01). By rotating the normal angle range corresponding to gestational age, the fetuses with CTD could not display views of their left ventricular long axis and main pulmonary trunk correctly. Conclusion: The left ventricular long axis and main pulmonary trunk views can be displayed using STIC so that the echocardiographic protocol of the cardiovascular joint could be standardized. The reference range of the angle between ascending aorta and main pulmonary artery is clinically useful in prenatal screening of CTD and provides a reliable quantitative standard to estimate the spatial relationship of the large arteries of fetus. Source


Wu S.,Linyi Peoples Hospital | Du X.,Women and Childrens Health Care Hospital of Linyi | Wu M.,Shaoxing Women and Childrens Hospital | Du H.,Shaoxing Women and Childrens Hospital | And 2 more authors.
Gene | Year: 2016

Osteosarcoma is the most common primary bone cancer which is associated with early metastatic potential and poor prognosis. However, the molecular mechanisms underlying osteosarcoma progression are not well characterized. Here, we investigated the role of miR-409-3p in osteosarcoma metastasis. Osteosarcoma tissue showed decreased expression of miR-409-3p compared to adjacent non-tumorous tissue. The expression level of miR-409-3p was negatively correlated with osteosarcoma metastasis. Overexpression of miR-409-3p in osteosarcoma cells (U2OS) inhibited cell migration and invasion. Bioinformatics analysis showed that catenin-δ1 (CTNND1, p120-catenin) is a direct target of miR-409-3p. Overexpression of miR-409-3p repressed the expression of catenin-δ1 in U2OS cells at both mRNA and protein levels. Meanwhile, miR-409-3p repressed the activity of luciferase reporter containing the 3'-untranslated region (3'UTR) of CTNND1 gene. Furthermore, expression of catenin-δ1 rescued the inhibitory effect of miR-409-3p on cell migration and invasion. Altogether, these results indicated that miR-409-3p targets catenin-δ1 to repress osteosarcoma metastasis. © 2016 Elsevier B.V. Source

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