Yunjun Xiao

Shenzhen Center for Disease Control and Prevention, Shen-ch’üan-shih, Zhejiang Sheng, China

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Publications (12)48.44 Total impact

  • International journal of cardiology 04/2014; · 7.08 Impact Factor
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    ABSTRACT: Dietary patterns are associated with plasma total homocysteine (tHcy) concentrations in healthy populations, but the associations between dietary protein and tHcy, total cysteine (tCys) in high risk populations are unclear. We therefore examined the association between dietary protein and tHcy and tCys concentrations in coronary angiographic subjects. We conducted a cross-sectional study of 1015 Chinese patients who underwent coronary angiography (40--85 y old). With the use of food-frequency questionnaires, we divided the total protein intakes into high animal-protein and high plant-protein diets. Circulating concentrations of tHcy and tCys were simultaneously measured by high-performance liquid chromatography with fluorescence detection. We found that high animal-protein diet was positively associated with hyperhomocysteinemia after adjustment for potential confounders, with the subjects in the highest quartile of intake having the greatest increase in risk (OR: 4.14, 95% CI: 2.67-6.43), whereas high plant-protein diet was inversely related to hyperhomocysteinemia, with a higher intake being protective. Compared with the first quartile of intake, the adjusted OR was 0.59 (95% CI: 0.38-0.91) for the fourth quartile. The total protein intake was positively associated with the risk of hypercysteinemia and the participants in highest quartile had significant OR of 1.69 (95% CI: 1.02-2.87) compared with those in lowest quartile. In multivariate linear regression analyses, high animal-protein and total-protein intakes were positively associated with plasma tHcy and tCys concentrations. The plant-protein intake was a negative determinant of plasma tHcy concentrations. High animal-protein diet was positively associated with high tHcy concentrations, whereas high plant-protein diet was inversely associated with tHcy concentrations. Furthermore the total protein intake was strongly related to tCys concentrations.
    Nutrition Journal 11/2013; 12(1):144. · 2.65 Impact Factor
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    ABSTRACT: Objective:Known diabetes is an independent predictor for mortality in coronary artery disease (CAD) patients, however, whether other glucose abnormalities are associated with death risk in CAD patients is unclear. The goal of this study was to examine the association between different glucose states and the risks of all-cause and cardiovascular disease (CVD) mortality among CAD patients.Research Design and Methods:The study cohort included 1726 CAD patients who were 40-85 years of age in the Guangdong Coronary Artery Disease Cohort. Cox proportional hazards regression models were used to estimate the association of baseline glucose status with risk of mortality.Results:During a median follow-up of 3.1 years, 129 deaths were recorded, 109 of which were due to CVD. The multivariable-adjusted (age, sex, education, marriage, leisure-time physical activity, smoking, alcohol drinking, body mass index, systolic blood pressure, total and high-density lipoprotein cholesterol, glomerular filtration rate, type, severity, duration, and treatment of CAD, history of heart failure, and use of antihypertensive, cholesterol-lowering, and anti-platelet drugs) hazard ratios in normoglycemia, impaired glucose regulation (IGR), newly diagnosed diabetes, and known diabetes were 1.00, 1.58 (95% CI 0.90-2.77), 2.41 (1.42-4.11), and 2.29 (1.36-3.84) for all-cause mortality, and 1.00, 1.89 (95% CI 1.01-3.54), 2.74 (1.50-5.01), and 2.73 (1.52-4.91) for CVD mortality. Assessing fasting plasma glucose only, impaired fasting glucose, newly diagnosed and known diabetes were also associated with increased risks of all-cause and CVD mortality compared with normoglycemia.Conclusions:CAD patients with IGR, newly diagnosed diabetes, and known diabetes have increased risk of CVD mortality.
    Diabetes care 10/2013; · 7.74 Impact Factor
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    ABSTRACT: Although cross-sectional studies have shown that plasma S-adenosylhomocysteine (SAH), the metabolic precursor of homocysteine, is associated with cardiovascular disease, the prospective relation between plasma SAH and cardiovascular disease risk is unknown. The aim of this study was to prospectively evaluate the association between plasma SAH and cardiovascular disease risk in coronary angiographic patients. Baseline plasma SAH and homocysteine concentrations were measured in 1003 patients aged between 21 and 87 y who underwent coronary angiography. Cox proportional hazards models were used to analyze the association between SAH and homocysteine and the risk of cardiovascular events, including fatal cardiovascular diseases, nonfatal myocardial infarction, and stroke. During the median follow-up period of 3.0 y, 93 participants developed cardiovascular events (32.7/1000 person-years). The age- and sex-adjusted hazard ratio of cardiovascular events was 3.38 (95% CI: 2.12, 5.39) for each 1-SD increase in the natural log-transformed SAH concentration. The age- and sex-adjusted hazard ratios of cardiovascular events across quartiles of SAH concentrations were 1.0, 2.25, 2.72, and 3.40 (P-trend = 0.007). Further adjustment for other cardiovascular disease risk factors and plasma homocysteine affected the results only slightly. This positive association between SAH and cardiovascular disease risk did not change when participants were stratified by age group, sex, and other baseline covariates. The results among a subset of participants with significant coronary stenosis were similar. Higher concentrations of plasma SAH are independently associated with an increased risk of cardiovascular events among patients undergoing coronary angiography. This trial was registered at as ChiCTR-RNRC-08000270.
    American Journal of Clinical Nutrition 09/2013; · 6.50 Impact Factor
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    ABSTRACT: Since universal salt iodization (USI) was implemented in Shenzhen, China, in 1996, evaluation of the time trend of USI to indicate the control of iodine-deficiency disorders has not been performed. To assess the time trend of median urinary iodine and total goiter rates from 1997 to 2011. Probability-proportionate-to-size sampling was employed in the surveillance of iodine-deficiency disorders, for which schoolchildren aged 8 to 10 years were randomly selected from five districts of the city during each iodine-deficiency disorders survey. Urinary iodine content and thyroid size were measured by ammonium persulfate oxidation and B ultrasound, respectively. The coverage of iodized salt increased from 73.2% in 1997 to more than 90% in 2011. The median urinary iodine of children aged 8 to 10 years varied between 207.1 and 278.8 microg/L; these levels were above the urinary iodine level in 1995. The proportion of urine samples with iodine content above 300 microg/L was 45.6% in 1997 and decreased to 20.8% in 2011, indicating excessive consumption of iodine by the children. The goiter rate among children dropped from 10.8% in 1997 to 1.3% in 2011; both values were lower than the goiter rate in 1995, indicating that the spread of endemic goiter was under control. Preliminary elimination of iodine-deficiency disorders was achieved by USI in Shenzhen. Nevertheless, some problems still existed, such as over-iodization. To clarify the causes of excessive urinary iodine content, the various sources of iodine from the diet need to be investigated in the future.
    Food and nutrition bulletin 09/2013; 34(3):331-7. · 2.11 Impact Factor
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    ABSTRACT: Fibroblast growth factor 23 (FGF23) is a circulating regulator of phosphate and vitamin D metabolism and is associated with coronary artery calcification, and has been implicated in the pathogenesis of cardiovascular disease. The aim of this study was to determine whether circulating FGF23 concentration is independently associated with the severity and extent of coronary artery disease in patients undergoing coronary angiography. A cross-sectional design was used to examine the relationship between serum FGF23 and the severity and extent of coronary artery stenosis in 2076 patients undergoing coronary angiography (1263 male and 813 female, mean aged 62.5 years). Subgroup analyses were performed to assess the associations between FGF23 and coronary arterial plaque characteristics evaluated by intravascular ultrasound and 12-month incidence of target vessel revascularization (TVR) and target lesion revascularization (TLR). We found a stepwise increase of serum FGF23 concentrations in patients with mild, moderate, severe stenosis or with increased number of stenotic vessels compared with those without stenosis (P<0.001). Serum FGF23 concentration was positively correlated with stenosis scores as the global index of the severity and extent of coronary artery stenosis in both male and female (r = 0.315 and r = 0.291, P<0.001). In multiple regression analyses, serum FGF23 concentration was a significant determinant of the stenosis scores independent of other traditional risk factors (standardized β = 0.326, P<0.001). Furthermore, subgroup analyses found FGF23 was significantly associated with plaque and dense calcium volumes. Multiple logistic regression analyses showed that serum FGF23 levels were significantly independent predictors of TVR and TLR. We report an independent association between circulating FGF23 concentration and the severity and extent of coronary artery stenosis in the coronary angiographic patients. Future studies are needed to elucidate the potential biological mechanisms and whether FGF23 is a modifiable cardiovascular risk factor.
    PLoS ONE 01/2013; 8(8):e72545. · 3.73 Impact Factor
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    ABSTRACT: The aim of the present study was to explore risk variants for coronary artery disease (CAD) and to evaluate their joint effects (quantified by genetic risk score; GRS) on the discrimination of CAD in a Chinese Han sample. An association analysis of 91 single nucleotide polymorphisms (SNPs) with CAD risk was undertaken in 1,007 CAD patients and 889 healthy controls. Two GRSs, counted GRS (cGRS) and weighted GRS (wGRS), were calculated using the significant SNPs, and their discriminant power for CAD was assessed using receiver-operating characteristic (ROC) curve analysis. Eight SNPs (rs11206510, rs10118757, rs2383206, rs501120, rs2075292, rs174547, rs173539, and rs255052) were nominally significantly associated with CAD (P<0.05), and 5 of them were newly reported. The GRSs derived from the 8 SNPs improved the discrimination of CAD compared to that using 4 conventional risk factors (P=0.002 for cGRS and P=0.009 for wGRS). After 10-fold cross-validation 100 times, the average areas under the curve were 0.668 (95% confidence interval [CI]: 0.667-0.669), 0.686 (95% CI: 0.685-0.687) and 0.690 (95% CI: 0.689-0.691) for models with conventional risk factors only, conventional risk factors plus cGRS, and conventional risk factors plus wGRS, respectively. A multigenic GRS, generated by combining multiple gene variants, can improve discrimination of CAD, thereby confirming the joint effects of these gene variants on CAD in this Chinese Han population.
    Circulation Journal 05/2012; 76(8):1987-92. · 3.58 Impact Factor
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    ABSTRACT: N-3 polyunsaturated fatty acids, such as docosahexaenoic acid (DHA; 22:6n-3), has clinical significance in the prevention and reversal of nonalcoholic steatohepatitis (NASH). However, the precious mechanism underlying remains unclear. The inflammasome, a multiprotein complex formed by NOD-like receptor (NLR) family members, has been recently shown to be activated in NASH and promote the cleavage of the pro-inflammatory cytokines to their maturation forms. HepG2 cells were exposed to different dose of PA for 24 h with or without the preincubation of 50 μM DHA for another 24 h and then lipid deposition was assessed with Oil red O staining and intracellular triglyceride (TG) determination. Secretory levels of inflammatory cytokines and Caspase-1 activity were determined by ELISA assays. Gene expression and protein levels were determined by quantitative RCR and western blotting, respectively. Palmitate (PA) dose-dependently increased lipid accumulation, TG content and induced the secretion of interleukin-1β (IL-1β), IL-18, TNF-α and MCP-1 from HepG2 cells. Preincubation with DHA significantly alleviated PA-induced lipid accumulation and inflammatory agents. DHA was also found to attenuate PA-induced NOD-like receptor protein 4 (NLRC4) mRNA expression. Furthermore, PA induced caspase-1 activation in a dose-dependent manner, resulting in exacerbating of procaspase-1 and pro-IL-1β processing. Knockdown of NLRC4 partially abrogated PA-induced caspase-1 activation and IL-1β maturation and completely abolished these events in the presence of DHA. Our findings indicate DHA attenuates PA-induced lipid accumulation and inflammation through suppressing NLRC4 inflammasome activation, caspase-1 activation and IL-1β cleavage.
    Nutrition & Metabolism 04/2012; 9(1):34. · 3.16 Impact Factor
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    ABSTRACT: Although S-adenosyl-homocysteine (SAH) is considered to be a more sensitive predictor of cardiovascular disease than homocysteine, the underlying mechanisms of its effects remain unknown. We investigated the in vivo and in vitro effects of SAH on vascular smooth muscle cells (VSMCs) proliferation and migration related to the development of atherogenesis in apolipoprotein E-deficient (apoE(-/-)) mice. A total of 72 apoE(-/-) mice were randomly divided into six groups (n= 12 for each group). The control group was fed a conventional diet, the M group was fed a 1% methionine-supplemented diet, the A group was fed a diet that was supplemented with the SAH hydrolase (SAHH) inhibitor adenosine-2, 3-dialdehyde (ADA), the M+A group was fed a diet that was supplemented with methionine plus ADA, and two of the groups were intravenously injected with retrovirus that expressed either SAHH shRNA (SAHH(+/-)) or scrambled shRNA semi-weekly for 8 weeks. Compared with the controls, the mice in the A, M+A, and SAHH(+/-) groups had higher plasma SAH levels, larger atheromatous plaques, elevated VSMC proliferation, and higher aortic reactive oxygen species and malondialdehyde levels. In cultured VSMCs, 5 μM ADA or SAHH shRNA caused SAH accumulation, which resulted in increased cell proliferation, migration, oxidative stress, and extracellular-regulated kinase 1/2 (ERK1/2) activation. These effects were significantly attenuated by preincubation with superoxide dismutase (300 U/mL). Our results suggest that elevated SAH induces VSMC proliferation and migration through an oxidative stress-dependent activation of the ERK1/2 pathway to promote atherogenesis.
    Cardiovascular research 04/2012; 95(2):241-50. · 5.80 Impact Factor
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    ABSTRACT: Cyanidin-3-glucoside (C3G) is a member of the anthocyanin family which belongs to the flavonoid class and possesses antiatherogenic properties. Many studies have demonstrated the protective effects of C3G on vascular endothelial cells and monocytes, however, the precise effects on vascular smooth muscle cells (VSMCs) have been less thoroughly studied. Hence, we investigated the role of C3G in TNF-α-induced VSMCs proliferation and explored the possible mechanisms. TNF-α stimulated VSMCs proliferation, and pretreatment with C3G inhibited the proliferation in dose- and time-dependent manners. Then, we found that C3G attenuated TNF-α-induced ROS over generation by Dihydroethidium staining. The combination of 50 μM C3G and 100 μM apocynin significantly reduced ROS generation. Moreover, C3G pretreatment significantly suppressed the expression of Nox activator 1, a subunit of NADPH oxidase in mouse VSMCs. C3G also inhibited TNF-α-induced signal transducer and activator of transcription (STAT3) phosphorylation, and the inhibitory effect was more prominent in C3G and apocynin co-pretreated cells than that pretreated with C3G or apocynin alone. Administration of the ROS scavenger catalase (2,000 U/ml) remarkably inhibited TNF-α-induced cell proliferation and STAT3 activation. These data suggest that C3G exerts its antiproliferative effect on TNF-α-induced VSMCs proliferation through inhibiting STAT3 activation by attenuating NoxA1-derived ROS over production.
    Molecular and Cellular Biochemistry 11/2011; 362(1-2):211-8. · 2.33 Impact Factor
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    ABSTRACT: Homocysteine and cysteine are considered as risk factors of cardiovascular disease. Homocysteine influences the liver expression of ApoA-I and decreases its blood level and HDL in genetic mice model. We aimed therefore to evaluate whether homocysteine and cysteine are associated with lipid parameters, and the joint effects of them on the risk of coronary artery disease (CAD). Plasma total homocysteine (tHcy), cysteine (tCys) and lipid markers were measured in 2058 consecutive coronary artery angiographic patients. Plasma tHcy but not tCys correlated negatively with ApoA-I (r = -0.153, P < 0.001) and with HDL cholesterol (r = -0.148, P < 0.001), and correlated positively with the risk of CAD (OR: 1.61; 95% confidence interval; 1.26 to 2.05). Combination of high tHcy and high tCys levels was associated with decreased ApoA-I and HDL cholesterol levels, and with increased risk of CAD (OR: 1.696, 95% CI (1.301-2.211)). Furthermore, low HDL cholesterol combined with low tHcy or high tHcy all had increased risk for CAD (OR: 1.254, 95% CI (1.114-1.565); OR: 1.332, 95% CI (1.093-1.624); respectively) whereas high HDL cholesterol counteracted the harmful effect of high tHcy on the risk of CAD. However, only the combination of high tHcy and high ApoA-I had an increased risk for CAD (OR: 1.438, 95% CI (1.170-1.768)). The association of homocysteine and cysteine, ApoA-I or HDL cholesterol and their joint effects provide new insights on its role on CAD.
    Lipids in Health and Disease 08/2011; 10:137. · 2.02 Impact Factor
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    ABSTRACT: Cyanidin-3-O-β-glucoside (Cy-3-g)-rich foods have been reported to inhibit the onset of obesity, but whether the pure anthocyanin supplementation affects obesity remains uncertain. Cy-3-g supplementation significantly reduced obesity, accumulation of fat in visceral adipose and liver tissues, and plasma triglyceride levels. Furthermore, adenosine monophosphate (AMP)-activated protein kinase phosphorylation (pAMPK) in the skeletal muscle and visceral adipose were significantly increased by Cy-3-g consumption. This was followed by the activation of lipoprotein lipase (LPL) in plasma and skeletal muscle but the suppression of this enzyme in visceral adipose. LPL activation in skeletal muscle cells and its suppression in adipocytes by Cy-3-g were blocked by inhibition of pAMPK. Our present data thus demonstrate that Cy-3-g improves obesity and triglyceride metabolism in KK-Ay mice. The underlying mechanism is found to be partly related to the activation of LPL in plasma and skeletal muscle, and inhibition of LPL in adipose tissue following the activation of pAMPK.
    Journal of the Science of Food and Agriculture 02/2011; 91(6):1006-13. · 1.76 Impact Factor

Publication Stats

35 Citations
48.44 Total Impact Points


  • 2013
    • Shenzhen Center for Disease Control and Prevention
      Shen-ch’üan-shih, Zhejiang Sheng, China
  • 2011–2013
    • Sun Yat-Sen University
      • • Department of Nutrition
      • • School of Public Health
      Guangzhou, Guangdong Sheng, China