Jun Cai

Capital Medical University, Peping, Beijing, China

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Publications (43)130.37 Total impact

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    ABSTRACT: Apoptosis is an important mechanism for the development of heart failure. Mitochondria are central to the execution of apoptosis in the intrinsic pathway. The main regulator of mitochondrial pathway of apoptosis is Bcl-2 family which includes pro- and anti-apoptotic proteins. MicroRNAs are small noncoding RNA molecules that regulate gene expression by inhibiting mRNA translation and/or inducing mRNA degradation. It has been proposed that microRNAs play critical roles in the cardiovascular physiology and pathogenesis of cardiovascular diseases. Our previous study has found that microRNA-181c, a miRNA expressed in the myocardial cells, plays an important role in the development of heart failure. With bioinformatics analysis, we predicted that miR-181c could target the 3' untranslated region of Bcl-2, one of the anti-apoptotic members of the Bcl-2 family. Thus, we have suggested that miR-181c was involved in regulation of Bcl-2. In this study, we investigated this hypothesis using the Dual-Luciferase Reporter Assay System. Cultured myocardial cells were transfected with the mimic or inhibitor of miR-181c. We found that the level of miR-181c was inversely correlated with the Bcl-2 protein level and that transfection of myocardial cells with the mimic or inhibitor of miR-181c resulted in significant changes in the levels of caspases, Bcl-2 and cytochrome C in these cells. The increased level of Bcl-2 caused by the decrease in miR-181c protected mitochondrial morphology from the tumour necrosis factor alpha-induced apoptosis. © 2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
    Journal of Cellular and Molecular Medicine 04/2015; DOI:10.1111/jcmm.12563 · 3.70 Impact Factor
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    ABSTRACT: Viral microRNAs (miRNAs) can regulate the host innate immune response. In particular, the human cytomegalovirus (HCMV) miRNA hcmv-miR-UL112 evades the host immune system by downregulating host immune gene and immediate-early viral gene expression. Natural killer (NK) cells are important innate immune cells with potent cytotoxicity, and are activated by type I interferons (IFNs) upon infection. It remains unclear how HCMV persists in the host despite the strongly antagonistic host immune system. A lentiviral vector was used to stably express hcmv-miR-UL112 in peripheral blood mononuclear cells (PBMCs). Hcmv-miR-UL112 expression levels were detected by TaqMan miRNA assay. The effects of hcmv-miR-UL112 on NK cell cytotoxicity were assessed with CD107a mobilization assay and CytoTox 96 non-radioactive cytotoxicity assay. Enzyme-linked immunosorbent assays (ELISA) were performed to detect type I IFNs levels in culture supernatants. To confirm the role of type I IFN in hcmv-miR-UL112-mediated NK cell cytotoxicity, PBMCs were incubated with antagonizing antibodies against IFN receptor (IFNAR) before lenti-hcmv-miR-UL112 treatment and recombinant type I IFN was added back into miR-transduced PBMC. Ectopically expressed hcmv-miR-UL112 functionally attenuated NK cell-mediated cytotoxicity, associated with decreased type I IFN expression. Hcmv-miR-UL112-transfected cells did not reduce the CD107-expression further than the IFNAR neutralizing mAbs-treatment alone, and adding back of recombinant type I IFN restored CD107a expression from the miR-transduced PBMC. Taken together, our results suggest that hcmv-miR-UL112 subverts innate immunity by downregulating type I IFN signaling to inhibit NK cell cytotoxicity. These results provide a new miRNA-based immunoevasion mechanism that may be exploited by HCMV.
    Immunology Letters 12/2014; 299(2). DOI:10.1016/j.imlet.2014.12.003 · 2.37 Impact Factor
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    ABSTRACT: Homocysteine (Hcy) is regarded as a risk factor for hypertension, but research on the causal relationship between Hcy and hypertension is limited. In the present study, we prospectively tracked the blood pressure progression of a normotensive population with different Hcy levels over a 2-year period. The incidence of hypertension with increasing Hcy quartiles produced an approximately U-shaped curve, with significance in males. Compared with the third quartile, the risk of hypertension in the first and second quartiles was increased by 1.55 (95% confidence interval [CI] 1.154-2.081) fold and 1.501 (95% CI 1.119-2.013) fold, respectively, with the increase being more significant in males. In conclusion, Hcy is related to hypertension incidence with the results approximating an U-shaped curve. Low Hcy levels might also increase the risk of hypertension.
    PLoS ONE 10/2014; 9(10):e108223. DOI:10.1371/journal.pone.0108223 · 3.53 Impact Factor
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    ABSTRACT: Chronic thromboembolic pulmonary hypertension (CTEPH) is a progressive disease characterized by misguided thrombolysis and remodeling of pulmonary arteries. MicroRNAs are small non-coding RNAs involved in multiple cell processes and functions. During CTEPH, circulating microRNA profile endued with characteristics of diseased cells could be identified as a biomarker, and might help in recognition of pathogenesis. Thus, in this study, we compared the differentially expressed microRNAs in plasma of CTEPH patients and healthy controls and investigated their potential functions. Microarray was used to identify microRNA expression profile and qRT-PCR for validation. The targets of differentially expressed microRNAs were identified in silico, and the Gene Ontology database and Kyoto Encyclopedia of Genes and Genomes pathway database were used for functional investigation of target gene profile. Targets of let-7b were validated by fluorescence reporter assay. Protein expression of target genes was determined by ELISA or western blotting. Cell migration was evaluated by wound healing assay. The results showed that 1) thirty five microRNAs were differentially expressed in CTEPH patients, among which, a signature of 17 microRNAs, which was shown to be related to the disease pathogenesis by in silico analysis, gave diagnostic efficacy of both sensitivity and specificity >0.9. 2) Let-7b, one of the down-regulated anti-oncogenic microRNAs in the signature, was validated to decrease to about 0.25 fold in CTEPH patients. 3) ET-1 and TGFBR1 were direct targets of let-7b. Altering let-7b level influenced ET-1 and TGFBR1 expression in pulmonary arterial endothelial cells (PAECs) as well as the migration of PAECs and pulmonary arterial smooth muscle cells (PASMCs). These results suggested that CTEPH patients had aberrant microRNA signature which might provide some clue for pathogenesis study and biomarker screening. Reduced let-7b might be involved in the pathogenesis of CTEPH by affecting ET-1 expression and the function of PAECs and PASMCs.
    PLoS ONE 06/2014; 9(6):e101055. DOI:10.1371/journal.pone.0101055 · 3.53 Impact Factor
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    ABSTRACT: The aim of this study was to investigate the effects of simvastatin on insulin secretion in mouse MIN6 cells and the possible mechanism. MIN6 cells were, respectively, treated with 0 μ M, 2 μ M, 5 μ M, and 10 μ M simvastatin for 48 h. Radio immunoassay was performed to measure the effect of simvastatin on insulin secretion in MIN6 cells. Luciferase method was used to examine the content of ATP in MIN6 cells. Real-time PCR and western blotting were performed to measure the mRNA and protein levels of inward rectifier potassium channel 6.2 (Kir6.2), voltage-dependent calcium channel 1.2 (Cav1.2), and glucose transporter-2 (GLUT2), respectively. ATP-sensitive potassium current and L-type calcium current were recorded by whole-cell patch-clamp technique. The results showed that high concentrations of simvastatin (5 μ M and 10 μ M) significantly reduced the synthesis and secretion of insulin compared to control groups in MIN6 cells (P < 0.05). ATP content in simvastatin-treated cells was lower than in control cells (P < 0.05). Compared with control group, the mRNA and protein expression of Kir6.2 increased with treatment of simvastatin (P < 0.05), and mRNA and protein expression of Cav1.2 and GLUT2 decreased in response to simvastatin (P < 0.05). Moreover, simvastatin increased the ATP-sensitive potassium current and reduced the L-type calcium current. These results suggest that simvastatin inhibits the synthesis and secretion of insulin through a reduction in saccharometabolism in MIN6 cells.
    Journal of Diabetes Research 06/2014; 2014:376570. DOI:10.1155/2014/376570 · 3.54 Impact Factor
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    ABSTRACT: To explore the prevalence of isolated diastolic hypertension and associated cardiovascular risk and blood pressure changes during follow up.
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    ABSTRACT: Blood pressure variability (BPV) is a reliable prognostic factor for cardiovascular events. Currently there is a worldwide lack of large sample size studies in visit-to-visit BPV. Based on the Kailuan Study, we analyzed the visit-to-visit BPV of patients to investigate the range and influencing factors of BPV. In 11 hospitals in the Kailuan Company, 4 441 patients received routine health checkups. Physical examination measured blood pressure (BP), body height, body weight, and waist circumference, and body mass index was calculated. Blood samples were analyzed for plasma total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), fasting blood glucose (FBG), and high-sensitivity c-reactive protein (hs-CRP). The effect of gender on systolic BPV was investigated. The average systolic BPV was 10.35 mmHg (1 mmHg = 0.133 kPa) overall, 10.54 mmHg in males and 10.06 mmHg in females. Multivariate Logistic regression analysis revealed that the age (RR = 1.022), systolic BP (SBP, RR = 1.007), LDL-C (RR = 1.098), and history of hypertension (RR = 1.273) were significant risk factors for higher systolic BPV. We found that aging (RR = 1.022), increased SBP (RR = 1.007), and a history of hypertension (RR = 1.394) were determinants of systolic BPV in males. The risk factors for systolic BPV of females were aging (RR = 1.017), increased SBP (RR = 1.009), increased LDL (RR = 1.136), and increased TG (RR = 1.157). Our findings indicated that the systolic BPV is closely associated with age, SBP and history of hypertension.
    Chinese medical journal 03/2014; 127(6):1022-6. · 1.02 Impact Factor
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    ABSTRACT: The American Heart Association has recently established seven ideal cardiovascular health metrics for cardiovascular health promotion and disease reduction (i.e., non-smoking, normal body mass index, physically active, healthy diet, and normal levels of cholesterol, blood pressure and fasting blood glucose). The present study seeks to evaluate how well these metrics predict mortality from all causes and cardiovascular diseases in adult Chinese living in a northern industrial city. Data of 95,429 adults who participated in the Kailuan cohort study from June 2006 to October 2007 was analyzed. All participants underwent questionnaire assessment, clinical examination, laboratory assessments and were followed up biannually. During a median follow-up of 4.02 years, 1,843 deaths occurred, with 597 deaths resulting from cardiovascular diseases. Lower mortality rates from all causes and cardiovascular diseases were observed among the subjects who met a higher number of the ideal health metrics. Compared to the participants who met none or one ideal health metric, those meeting ≥5 ideal health metrics had a lower risk of all-cause mortality by 30% (adjusted hazard ratio, 0.70; 95% confidence interval, 0.56-0.88) and a lower risk of mortality from cardiovascular diseases by 39% (adjusted hazard ratio, 0.61; 95% confidence interval, 0.41-0.89) . Four metrics (smoking status, physical activity, blood pressure and fasting blood glucose) were significantly associated with all-cause mortality. Three metrics (physical activity, blood pressure and fasting blood glucose) were significantly associated with mortality from cardiovascular diseases. The number of ideal health metrics is negatively associated with mortality rates from all causes and cardiovascular diseases among adults in a Northern Chinese industrial city. The data supports the AHA recommendation of ideal health metrics for adults from Northern China.
    PLoS ONE 02/2014; 9(2):e89161. DOI:10.1371/journal.pone.0089161 · 3.53 Impact Factor
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    ABSTRACT: Recent genome-wide association (GWA) studies in Caucasians identified multiple single nucleotide polymorphisms (SNPs) associated with coronary artery disease (CAD). The associations of those SNPs with myocardial infarction (MI) have not been replicated in Asian populations. Among those previously identified SNPs, we selected nine (rs10953541, rs1122608, rs12190287, rs12413409, rs1412444, rs1746048, rs3798220, rs4977574, rs579459, in or near genes 7q22, LDLR, TCF21, CYP17A1, LIPA, CXCL12, LPA, CDKN2A, ABO, respectively) because of the relatively high minor allele frequencies in Chinese individuals and tested the associations of the SNPs with MI and MI related risk factors in Chinese population. We conducted a case-control association study on a cohort of 2365 MI patients and 2678 unrelated controls from the Chinese population. Genotyping of 9 SNPs were performed by the TaqMan Real Time PCR method. After age, sex, and BMI adjustment, we observed the SNPs rs12190287, rs12413409, rs1412444, rs1746048 and rs4977574, were significantly associated with MI in additive models and rs12190287, rs12413409, rs4977574 were significantly associated with phenotypes of MI at the same time. We also found three SNPs rs1122608, rs3798220 and rs579459 were significantly associated with risk factors of MI, although they had no association with MI in Chinese population. Results of this study indicate that 5 SNPs were associated with MI and 3 SNPs were associated with associated with lipoprotein levels but not with MI in a Chinese population. The present study supports some CAD-related genes in Caucasian as important genes for MI in a Chinese population.
    PLoS ONE 01/2014; 9(1):e86332. DOI:10.1371/journal.pone.0086332 · 3.53 Impact Factor
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    ABSTRACT: Objectives: The present study was designed to decipher the molecular mechanisms underlying angiotensin (Ang) II-induced overexpression of connective tissue growth factor (CTGF) in cultured cardiomyocytes. Methods: Cardiomyocytes isolated from 1- to 3-day-old neonatal rats were cultured and treated with 100 nM Ang II with or without pretreatment with 10 nM telmisartan, an Ang II type 1 receptor antagonist. The role of microRNA (miR)-19b in the regulation of Ang II-induced CTGF expression was evaluated in cultured cardiomyocytes with quantitative real-time reverse transcription polymerase chain reaction and Western blot analysis. Results: We provide several lines of evidence to show that miR-19b contributes to the Ang II-induced overexpression of CTGF in cultured cardiomyocytes. Firstly, administration of Ang II decreased the level of miR-19b dramatically (p < 0.05 vs. control), which was abolished by telmisartan. Secondly, Ang II increased the level of CTGF significantly (p < 0.05 vs. control), which was also prevented by pretreatment with telmisartan. Thirdly, overexpression of miR-19b decreased CTGF levels (p < 0.05 vs. control). Finally, transfection of miR-19b into cardiomyocytes prevented the upregulation of CTGF induced by Ang II. Conclusion: Downregulation of miR-19b contributes to Ang II-induced overexpression of CTGF in cultured cardiomyocytes. © 2013 S. Karger AG, Basel.
    Cardiology 11/2013; 127(2):114-120. DOI:10.1159/000355429 · 2.04 Impact Factor
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    ABSTRACT: To investigate the impact of resting heart rate (RHR) on new-onset diabetes (NOD) in population without hypertension. This prospective cohort study was performed in 2006 and 2007 and screened 101 510 participants. All subjects were employees of the Kailuan Group, a state-run coal mining company. The observation cohort included 48 926 subjects with normal fasting blood glucose (FBG) <7.0 mmol/L, no history of diabetes, complete FBG and RHR examination data, systolic blood pressure <140 mm Hg (1 mm Hg = 0.133 kPa) , diastolic blood pressure <90 mm Hg, no history of hypertension, and no use of hypoglycemic agents or antihypertensive drugs.We excluded participants without a health examination in 2008-2009 or 2010-2011 and those with incomplete examination data. A total of 29 910 participants were included in the final analysis. The observation population was divided into four groups according to RHR data collected during 2006-2007 health examinations: quartile 1 (RHR<63 beats/min) ; quartile 2 (63 beats/min ≤ RHR<70 beats/min) ; quartile 3 (70 beats/min ≤ RHR<75 beats/min) ; quartile 4 ( RHR ≥ 75 beats/min). Kaplan-Meier analysis was used to calculate the incidence of NOD. The relationship between RHR and NOD was estimated using Cox proportional hazard analysis. The incidences of NOD/1000 person-years for the above quartiles of RHR were 11.22, 13.58, 13.96, and 17.55, respectively in the total observational population; the corresponding incidences were 12.17, 15.20, 16.08, 20.44, and 8.29, 9.38, 8.86, and 9.60 in men and women, respectively. Compared with quartile 1, Cox proportional hazard regression analysis showed that the other three RHR groups had an increased risk of NOD after adjusting for age, gender, systolic blood pressure, diastolic blood pressure, and other risk factors. The hazard ratio values for these groups were 1.20 (95%CI:1.04-1.40, P < 0.05), 1.25 (95%CI:1.07-1.45, P < 0.01) and 1.58 (95%CI:1.36-1.82, P < 0.01), respectively.Furthermore, after adjusted the FBG, risk of NOD was significantly higher in quartile 2 (HR = 1.21, 95%CI:1.04-1.40, P < 0.01) and quartile 4 (HR = 1.22, 95%CI:1.06-1.41, P < 0.01 compared that in quartile 1. After adjusting for the factors listed above, the influence of RHR on NOD was not significant in women (P > 0.05) , but there was still an increased risk of NOD in men compared with quartile 1 with hazard ratio values of 1.21 (95%CI:1.02-1.43, P < 0.05) , and 1.27 (95%CI:1.09-1.49, P < 0.01) for quartile 2 and quartile 4, respectively. Higher RHR is linked with higher risk of NOD in population without hypertension.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 11/2013; 41(11):968-73.
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    ABSTRACT: Micro-RNAs regulate gene expression by directly binding to the target mRNAs. The goal of the study was to examine the expression profiling of miRNAs in human failing hearts and identify the key miRNAs that regulate molecular signalling networks and thus contribute to this pathological process. The levels of miRNAs and expressed genes were analysed in myocardial biopsy samples from patients with end-stage heart failure (n = 14) and those from normal heart samples (n = 8). Four networks were built including the Gene regulatory network, Signal-Network, miRNA-GO-Network and miRNA-Gene-Network. According to the fold change in the network and probability values in the microarray cohort, RT-PCR was performed to measure the expression of five of the 72 differentially regulated miRNAs. miR-340 achieved statistically significant. miR-340 was identified for the first time in cardiac pathophysiological condition. We overexpressed miR-340 in cultured neonatal rat cardiomyocytes to identify whether miR-340 plays a determining role in the progression of heart failure. ANP, BNP and caspase-3 were significantly elevated in the miR-340 transfected cells compared with controls (P < 0.05). The cross-sectional area of overexpressing miR-340 cardiomyocytes (1952.22 ± 106.59) was greater (P < 0.0001) than controls (1059.99 ± 45.59) documented by Laser Confocal Microscopy. The changes of cellular structure and the volume were statistical significance. Our study provided a comprehensive miRNA expression profiling in the end-stage heart failure and identified miR-340 as a key miRNA contributing to the occurrence and progression of heart failure. Our discoveries provide novel therapeutic targets for patients with heart failure.
    Journal of Cellular and Molecular Medicine 09/2013; 17(9). DOI:10.1111/jcmm.12096 · 3.70 Impact Factor
  • International journal of cardiology 07/2013; 168(4). DOI:10.1016/j.ijcard.2013.06.111 · 6.18 Impact Factor
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    ABSTRACT: To observe the impact of systolic blood pressure (SBP) on visit-to-visit blood pressure variability (BPV) in middle-aged and elderly people. Visit-to-visit BPV was determined in 5440 workers in the Kailuan study cohort from 2006 to 2007. The subjects were ≥ 40 years-old and had no history of stroke, transient ischemic attack or myocardial infarction. Participants were divided into five groups according to different levels of SBP. Linear regression was used to analyze the related factors which might affect BPV. Mean systolic BPV of all subjects was 10.35 mm Hg [coefficient of variation (CV 7.96%)]. The mean systolic BPV of males was 10.54 mm Hg (CV 7.90%) while the mean SBPV of females was 10.06 mm Hg (CV 7.90%). The BPV of males was significant higher than that of females (P < 0.001). CV of SBP was similar between males and females. Furthermore, higher SBP was associated with higher BPV. There were significant differences in BPV between different groups with different levels of SBP (P < 0.001). Linear regression analysis demonstrated that SBP, age, gender, high-sensitivity C-reactive protein (hsCRP) were affecting factors of BPV. Twenty mm Hg SBP increase was linked with 2.02 mm Hg BPV increase and 0.388%CV increase. Age increase of 1 year was associated with 0.044 mm Hg BPV increase and 0.029% CV increase. SBP, age, gender and hsCRP are important factors affecting BPV in middle-aged and elderly people. Higher SBP is closely related to greater BPV in this cohort.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 03/2013; 41(3):219-23.
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    ABSTRACT: Micro‐RNAs regulate gene expression by directly binding to the target mRNAs. The goal of the study was to examine the expression profiling of miRNAs in human failing hearts and identify the key miRNAs that regulate molecular signalling networks and thus contribute to this pathological process. The levels of miRNAs and expressed genes were analysed in myocardial biopsy samples from patients with end‐stage heart failure (n = 14) and those from normal heart samples (n = 8). Four networks were built including the Gene regulatory network, Signal‐Network, miRNA‐GO‐Network and miRNA‐Gene‐Network. According to the fold change in the network and probability values in the microarray cohort, RT‐PCR was performed to measure the expression of five of the 72 differentially regulated miRNAs. miR‐340 achieved statistically significant. miR‐340 was identified for the first time in cardiac pathophysiological condition. We overexpressed miR‐340 in cultured neonatal rat cardiomyocytes to identify whether miR‐340 plays a determining role in the progression of heart failure. ANP, BNP and caspase‐3 were significantly elevated in the miR‐340 transfected cells compared with controls (P P Document Type: Research Article DOI: http://dx.doi.org/10.1111/jcmm.12096 Publication date: September 1, 2013 $(document).ready(function() { var shortdescription = $(".originaldescription").text().replace(/\\&/g, '&').replace(/\\, '<').replace(/\\>/g, '>').replace(/\\t/g, ' ').replace(/\\n/g, ''); if (shortdescription.length > 350){ shortdescription = "" + shortdescription.substring(0,250) + "... more"; } $(".descriptionitem").prepend(shortdescription); $(".shortdescription a").click(function() { $(".shortdescription").hide(); $(".originaldescription").slideDown(); return false; }); }); Related content In this: publication By this: publisher In this Subject: Biology , Medicine By this author: Zhu, Xiaoming ; Wang, Hongjiang ; Liu, Fan ; Chen, Li ; Luo, Weijia ; Su, Pixiong ; Li, Weiming ; Yu, Liping ; Yang, Xinchun ; Cai, Jun GA_googleFillSlot("Horizontal_banner_bottom");
    Journal of Cellular and Molecular Medicine 01/2013; 17(9). · 3.70 Impact Factor
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    ABSTRACT: OBJECTIVES: This study aimed to determine the occurrence of cardiovascular (CV) events in a prehypertensive Chinese population. METHODS: Participants meeting the JNC 7 diagnostic criteria for prehypertension (n=30,027) and ideal blood pressure (n=15,614) were enrolled in this prospective, observational cohort. New CV events were collected during follow-up of 38-53months (mean 47.58±3.19months). A multivariate Cox proportional hazard regression model was used to analyze factors influencing CV events. RESULTS: Four hundred sixty-one CV events occurred during the follow-up period. Cumulative incidence rates for total CV events, cerebral infarct, cerebral hemorrhage, myocardial infarct, and deaths due to CV in the prehypertensive population were 1.19%, 0.57%, 0.20%, 0.23%, and 0.23%, respectively. These rates were higher than those of the ideal blood pressure group (0.67%, 0.27%, 0.12%, 0.17%, and 0.15% respectively). After correcting for traditional CV risk factors, relative risks (RRs) for total CV events, cerebral infarct and cerebral hemorrhages in the prehypertensive population were 1.32 (95% confidence intervals (CI): 1.06-1.65), 1.55 (95% CI: 1.10-2.18) and 1.40 (95% CI: 0.82-2.37) higher than those in the ideal blood pressure population. Compared to the ideal blood pressure group, the prehypertensive population was older, more likely male, and had higher triglycerides, total cholesterol, low-density lipoprotein cholesterol, and body mass index (p<0.05). CONCLUSION: Prehypertension is an independent risk factor for total CV events and stroke.
    International journal of cardiology 07/2012; 167(5). DOI:10.1016/j.ijcard.2012.05.123 · 6.18 Impact Factor
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    ABSTRACT: The American Heart Association Committee recently developed definitions of "ideal," "intermediate," and "poor" cardiovascular health based on 7 cardiovascular disease (CVD) risk factors or health behaviors. This study evaluated the prevalence of "ideal" American Heart Association cardiovascular health metrics from June 2006 to October 2007 in the Kailuan cohort (n=101 510; age 18-98 years) in northern China and its relationship with the 4-year CVD incidence. We used Cox proportional hazards regression to calculate hazard ratios and 95% confidence intervals for baseline health behaviors and risk factor categories. The majority of participants (63,676; 69.45%) presented with ≤3 ideal cardiovascular health metrics, whereas 8342 participants (9.1%) had 5 to 7 ideal metrics. Only 93 of 91,698 participants (0.1%) had all 7 metrics in the ideal range. There was a strong relationship between the cumulative incidence of CVD events in the 4-year follow-up and the number of ideal health metrics at baseline; the 1111 participants with 6 and 7 ideal metrics had a significantly lower cumulative incidence of CVD than subjects with no or only 1 ideal health metric (0.8% versus 3.3%). Men had higher rates of CVD events than women (2.46% versus 1.18%). Few adults had ideal cardiovascular health according to the modified American Heart Association definition. We detected a strong inverse relationship between the cumulative CVD incidence and the number of ideal health metrics at baseline. Population-wide prevention, especially lifestyle improvement, is critical to increase the low-risk prevalence and thereafter decrease CVD events. Clinical Trial Registration- URL: http://www.chictr.org/cn/proj/show.aspx?proj=1441. Unique identifier: ChiCTR-TNC-11001489.
    Circulation Cardiovascular Quality and Outcomes 07/2012; 5(4):487-93. DOI:10.1161/CIRCOUTCOMES.111.963694 · 5.04 Impact Factor
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    ABSTRACT: An insertion/deletion (I/D) variant in the angiotensin-converting enzyme (ACE) gene was associated with ACE inhibitor (ACEI)-related cough in previous studies. However, the results were inconsistent. Our objective was to assess the relationship between the ACE I/D polymorphism and ACEI-related cough by meta-analysis and to summarize all studies that are related to ACE I/D polymorphism and ACEI-cough and make a summary conclusion to provide reference for the researchers who attempt to conduct such a study. Databases including PubMed, EMbase, Cochrane Library, and China National Knowledge Infrastructure, were searched for genetic association studies. Data were extracted by two independent authors and pooled odds ratio (OR) with 95% confidence interval (CI) was calculated. Metaregression and subgroup analyses were performed to identify the source of heterogeneity. Eleven trials, including 906 cases (ACEI-related cough) and 1,175 controls, were reviewed in the present meta-analysis. The random effects pooled OR was 1.16 (95%CI: 0.78-1.74, p=0.46) in the dominant model and 1.61 (95%CI: 1.18-2.20, p=0.003) in the recessive model. Heterogeneity was found among and within studies. Metaregression indicated that the effect size was positively associated with age and negatively associated with follow-up duration of ACEI treatment. Subgroup analysis revealed a significant association between ACE I/D polymorphism and ACEI-related cough in studies with mean age >60 y, but not in studies with mean age ≤ 60 y. No heterogeneity was found within each mean age subgroup. We also found no association between ACE I/D polymorphism and ACEI-related cough in studies with follow-up>2 mo or in studies in Caucasians. No heterogeneity was detected in these two subgroups. Synthesis of the available evidence supports ACE I/D polymorphism as an age-dependent predictor for risk of ACEI-related cough.
    PLoS ONE 06/2012; 7(6):e37396. DOI:10.1371/journal.pone.0037396 · 3.53 Impact Factor
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    ABSTRACT: Human cytomegalovirus (HCMV) is implicated in several cardiovascular disorders, including atherosclerosis, coronary heart disease, and cardiac transplant arteriopathy. We aimed to evaluate the relationship between HCMV and stroke. Real-time polymerase chain reaction (PCR) and ELISA were performed on plasma samples isolated from 200 patients diagnosed with stroke and 200 controls. All participants belonged to the Stroke Hypertension Investigation in Genetics (SHINING) study. HCMV seropositivity was higher in the stroke group than in controls (55.0% vs. 23.5%; P < 0.0001). The presence of HCMV DNA increased the risk of stroke (unadjusted odds ratio [OR], 3.98; 95% confidence interval [CI], 2.59 to 6.11; P < 0.0001). Risks were also increased for the subtypes ischemic stroke (unadjusted OR, 4.01; 95% CI, 2.57-6.24; P < 0.0001) and hemorrhagic stroke (unadjusted OR, 3.80; 95% CI, 1.64-8.78; P= 0.0018). Increased risk with HCMV remained significant after adjustment for age, sex, body mass index, hypertension, and smoking (ischemic stroke: adjusted OR, 4.07; 95% CI, 2.52-6.32; P < 0.0001; hemorrhagic stroke: adjusted OR, 3.88; 95% CI, 1.61-9.36; P= 0.0026). We demonstrate a novel link between HCMV infection and stroke. These findings may provide important insights into the pathogenesis of stroke.
    CNS Neuroscience & Therapeutics 06/2012; 18(6):457-60. DOI:10.1111/j.1755-5949.2012.00326.x · 3.78 Impact Factor
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    ABSTRACT: This study investigated the impact of metabolic syndrome on the development of cardio-cerebral vascular (CVD) events in a pre-hypertensive population. The data used in this prospective study was derived from the Kailuan study cohort (n = 101 510). Prehypertension was diagnosed in 29 968 (mean age: 50 ± 9 years and 23 744 males) individuals by the JNC VII criteria and these subjects were further classified into metabolic syndrome positive (MS+, n = 3447) and MS negative (MS-, n = 26 521) groups according to the modified 2004 Chinese Diabetes Society criteria. Subjects were followed up for 38 - 53 (mean 47 ± 5) months and first-ever CVD events were recorded. Baseline anthropometric and laboratory features were obtained by physical examination from June 2006 to October 2007 and the last follow-up day was December 31, 2010. Multivariable Cox proportional hazards regression models were used to analyze the risk factors of first-ever CVD events. There were 354 CVD events during follow up. The incidences of CVD events (1.80% vs. 1.28%) and cerebral infarction (1.10% vs. 0.57%) were significantly higher in the MS+ group than in the MS- group (all P < 0.05). After adjustment for other established CVD risk factors, the hazards ratio was 1.45 (95%CI: 1.10 - 1.92) for total CVD events and 1.84 (95%CI: 1.27 - 2.67) for cerebral infarction events in MS+ group. In this cohort, metabolic syndrome is linked with increased risk for CVD events.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 05/2012; 40(5):397-401.

Publication Stats

331 Citations
130.37 Total Impact Points

Institutions

  • 2008–2014
    • Capital Medical University
      • Department of Cardiology
      Peping, Beijing, China
  • 2012
    • Shantou University
      • Department of Cardiology
      Swatow, Guangdong, China
    • Xiamen University
      Amoy, Fujian, China
    • Hebei University
      Pao-ting-shih, Hebei, China
  • 2009–2010
    • Harvard Medical School
      Boston, Massachusetts, United States
    • Harvard University
      Cambridge, Massachusetts, United States
  • 2006–2007
    • Renmin University of China
      Peping, Beijing, China