Ying-Zhong Lin

Maternal and Children Health Hospital of Guangxi Zhuang Autonomous Region, Yung-ning, Guangxi Zhuangzu Zizhiqu, China

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Publications (6)8.73 Total impact

  • Ying Huang, Ying-Zhong Lin, Ying Shi, Qing-Wei Ji
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    ABSTRACT: The imbalance of anti- inflammatory/pro-inflammatory cytokines plays an important role in the process of atherosclerosis. IL-35 is an anti-inflammatory cytokine comprising the p35 subunit of IL-12 and the subunit Epstein-Barr virus (EBV) -induced gene 3(EBI3). Accumulating evidence showed that IL-35 up-regulates the expression of anti-inflammatory cytokines, induces the generation of CD4 + regulatory T cells, inhibits CD4 + effector T cells response and other target cells activity, and reduces the progression of inflammatory and autoimmune diseases. In addition, it has been found that Ebi3 and p35 strongly coexpressed in human advanced lesions. Therefore, we hypothesize that IL-35 may become a novel target for the treatment of atherosclerosis. Further studies are required to investigate the precise effect and the signaling pathway of IL-35 in atherosclerosis process.
    Pharmazie 10/2013; 68(10):793-5. · 0.96 Impact Factor
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    ABSTRACT: Background. Regulatory T (Treg) cells play a protective role in atherosclerosis prone models and are related to the onset of acute coronary syndromes (ACS, including non-ST-elevation ACS (NSTEACS) and ST-elevation acute myocardial infarction (STEAMI)). CD4+LAP+ Treg cells are a novel subset of Tregs that have been found to ameliorate atherosclerosis in ApoE(-/-) mice, and these cells also exist in humans. The present study was designed to investigate whether CD4+LAP+ Treg cells are involved in the onset of ACS. Methods. The frequencies of CD4+LAP+ and CD4+CD25+ Treg cells were detected using flow cytometric analysis, and the plasma IL-10 and TGF- β 1 levels were measured using an ELISA in 29 stable angina (SA) patients, 30 NSTEACS patients, 27 STEAMI patients, and a control group (30 cases). Results. The results revealed a significant decrease in the frequencies of CD4+LAP+ and CD4+CD25+ Treg cells and in the levels of IL-10 and TGF- β 1 in patients with ACS compared with those in the SA and control groups. Conclusions. The decrease in the frequencies of CD4+LAP+ and CD4+CD25+ Treg cells may play a role in the onset of ACS.
    Mediators of Inflammation 01/2013; 2013:764082. · 3.88 Impact Factor
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    ABSTRACT: Background. CD4+ T helper (Th) cells play critical roles in the development and progression of atherosclerosis and the onset of acute coronary syndromes (ACS, including acute myocardial infarction (AMI) and unstable angina pectoris (UAP)). In addition to Th1, Th2, and Th17 cells, Th22 and Th9 subsets have been identified in humans. In the present study, we investigated whether Th22 cells and Th9 cells are involved in the onset of ACS. Methods. The frequencies of Th22 and Th9 cells were detected using a flow cytometric analysis and their related cytokine and transcription factor were measured in the AMI, UAP, stable angina pectoris (SAP), and control groups. Results. The results revealed a significant increase in the peripheral Th22 number, AHR expression, and IL-22 levels in patients with ACS compared with those in the SAP and control groups. Although there was no difference in the peripheral Th9 number among the four groups, the PU.1 expression and IL-9 levels were significantly increased in patients with ACS compared with the SAP and control groups. Conclusions. Circulating Th22 and Th9 type responses may play a potential role in the onset of ACS symptom.
    Mediators of Inflammation 01/2013; 2013:635672. · 3.88 Impact Factor
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    ABSTRACT: To explore the role of microRNA-92a (miR-92a) in evaluating endothelium damage induced by percutaneous coronary intervention (PCI). A case control study was prospectively conducted. Fifty-eight patients with ST-segment elevation acute myocardial infarction (STEAMI) received PCI were enrolled. MiR-92a expression in circulation was determined on the next day after PCI (reverse transcription-polymerase chain reaction). The correlation between miR-92a expression in circulation and PCI influence factors, such as inflation pressure, duration of balloon inflation and length of culprit atheromatous plaque were explored. MiR-92a was lower in inflation pressure 11-19 atm (1 atm=101.325 kPa) group [n=43, mean -0.36, 95% confidence interval (95%CI) -0.60 to -0.12] than inflation pressure ≤10 atm group (n=11, mean 1.16, 95%CI 0.80 to 1.52, P<0.01) and ≥ 20 atm group (n=4, mean 0.26, 95%CI 0.26 to 0.26, P=0.1); and also lower in duration of balloon inflation 6-7 seconds group (n=24, mean -0.42, 95%CI -0.83 to -0.01) than in duration of balloon inflation ≤ 5 seconds group (n=9, mean 0.63, 95%CI 0.49 to 0.78, P=0.03) and ≥ 8 seconds group (n=25, mean 0.45, 95%CI 0.10 to 0.80, P<0.001); lower in implanted stent length ≤30 mm (n=31, mean -0.48, 95%CI -0.80 to -0.16) than those >30 mm (n=27, mean 0.16, 95%CI 0.01 to 0.32, P<0.01). A significantly negative correlation was found between inflation pressure and duration of balloon inflation. (r=-0.48, P<0.001). There is a relationship between circulating miR-92a, inflation pressure and duration of balloon inflation. Circulating miR-92a could be used to evaluate the endothelium injury induced by PCI, and be used as a new target of prevention and treatment of endothelial dysfunction following revascularization.
    Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue 12/2012; 24(12):721-4.
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    ABSTRACT: To investigate the modulatory function of statin therapy on circulating microRNA-92a (miR-92a) in patients with coronary heart disease (CHD), and to evaluate the possibility of miR-92a as a new target of treatment for endothelial dysfunction. A case control study was conducted. Prevalence of abnormal blood fat content, statin treatment rate, and attainment rate of low density lipoprotein-cholesterol (LDL-C) lowered to expected level in 236 patients with CHD were analyzed. Relationship between statin therapy in patients with type 2 diabetes mellitus (DM), and level of LDL-C and circulating miR-92a expression was analyzed by multivariate general linear factorial analysis. The incidence of acute coronary syndrome (ACS) was compared in patients with CHD receiving statin therapy in all groups. Prevalence of abnormal LDL-C was 95.7% (112/117) in CHD patients of non-statin therapy group, and 47.5% (112/236) of patients with CHD who should receive statin therapy but did not. Attainment rate of lowering of LDL-C to expected level in statin therapy group was 27.7% (33/119). LDL-C level (mmol/L) was significantly lower in statin therapy group than that in non-statin therapy group (2.457 ± 0.802 vs. 3.218 ± 1.130, Z = -9.760, P = 0.001), and incidence of ACS was significantly lower in statin therapy group than that in non-statin therapy group [33.6% vs. 71.8%, χ(2) = 34.491, P = 0.001]. There was no significant difference in incidence of ACS between patients with or without attaining the expected low value of LDL-C in statin therapy group [33.3% vs. 33.7%,χ(2) = 0.002, P = 0.968]. Circulating miR-92a expression was significantly higher in patients with stable angina pectioris (SAP) complicated with DM than those without DM (0.492 vs. -0.121, Z = -3.038, P = 0.002). It was found that statin therapy could down regulate miR-92a expression in patients with SAP complicated with DM as compared with that with non-statin therapy (0.419 vs. 0.687, Z = 1.289, P = 0.072). There was no significant difference in circulating miR-92a expression between statin therapy and non-statin therapy in patients with SAP without co-existing DM (-0.032 vs. -0.198, Z = -0.614, P = 0.539). Multivariate general linear factorial analysis showed that statin therapy was the major influential factor on LDL-C level in patients with CHD (F = 22.863, P = 0.001), and complicating DM was the major influential factor on circulating miR-92a expression in patients with SAP (F = 9.641, P = 0.003). Regulation of circulating miR-92a expression may be considered as a new clinical target for statin treating endothelial dysfunction in patients with CHD.
    Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue 04/2012; 24(4):215-8.
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    ABSTRACT: To examine the expression of circulating microRNA-92a (miR-92a) in patients with ST-segment elevation myocardial infarction (STEMI), and the impact of percutaneous coronary intervention (PCI) on such expression. The level of circulating miR-92a was measured in three groups of patients: 58 STEMI patients received PCI, 24 STEMI patients received no PCI, and 116 patients with stable angina pectoris (SAP) without PCI. On the day next to admission, STEMI patients received no PCI were found to have higher level of circulating miR-92a as compared to SAP patients without PCI (0.2869 ± 0.8167 vs. -0.0555 ± 0.9855, F = 2.438, P = 0.121). Twenty-four hours after the PCI, the level of circulating miR-92a in STEMI patients received the procedure was lower than those without it (-0.0324 ± 0.9563 vs. 0.2869 ± 0.8167, F = 2.054, P = 0.156). The SAP patients (without PCI) had higher survival rate as compared to the STEMI patients without PCI (100.0% vs. 75.0% P = 0.001), and the survival rate in STEMI patients received PCI was higher than those without it (89.7% vs. 75.0%, P = 0.088). In STEMI patients, the expression of circulating miR-92a is up-regulated. PCI therapy may suppress such up-regulation. Survival rate is higher in patients showing down-regulation of miR-92a. Our data suggest that miR-92a might have potential for diagnosis and therapeutic application in the prevention and treatment of STEMI.
    Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue 12/2011; 23(12):718-22.