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Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: CX3CL1 played an important role in atherosclerosis recently. We investigated the association between the chemokine CX3CL1 with coronary artery disease in type 2 diabetes mellitus. Methods: CX3CL1 expression in carotid artery specimens was analysed by immunohistochemistry. The study was conducted in 400 coronary artery disease in type 2 diabetes mellitus and 400 control subjects in a case-control study. CX3CL1 gene rs170364 variant was detected by the directing sequencing technology. Results: CX3CL1 expressions were increased markedly in carotid artery plaque than in normal carotid artery. CX3CL1 gene rs170364 genotype (GG, GT and TT) frequency in coronary artery disease in type 2 diabetes mellitus is 42.7%, 40.0% and 17.2%, and 50.2%, 39.6% and 10.2% in the control group. CX3CL1 gene rs170364 variant is a genetic risk factor for coronary artery disease in type 2 diabetes mellitus (P <0.05). Logistic regression analysis with adjustments for other risk factors showed that the CX3CL1 gene rs170364 T allele significantly increases the risk of coronary artery disease in type 2 diabetes mellitus compared with the control subjects (P <0.05). Conclusion: Our study shows that the CX3CL1 expression increased in the carotid plaques and serum of the coronary artery disease in type 2 diabetes mellitus. CX3CL1 gene rs170364 variant may be considered a genetic risk factor for coronary artery disease in type 2diabetes mellitus. [ABSTRACT FROM AUTHOR]

Objective: To explore the clinical significance of serum CX3CL1 level for coronary artery disease. Methods: The study was conducted in 250 cases of coronary artery disease patients(75 patients with stable angina pectoria,75 patients with unstable angina pectoris,50 patients with ST-elevation acute myocardial infarction,50 non ST-elevation acute myocardial infarction patients) and 200 cases of control subjects(normal coronay artery) in a case-control study. The CX3CL1 level in different groups were analyzed by ELISA and CX3CR1 expression on CD4~+CD28~-T cells was analyzed by flow cytometry. Results: The serum CX3CL1 level increased markedly in coronary artery disease patients compared with the control subjects(P<0.05). The serum CX3CL1 level of patients with stable unstable angina was increased in the patients with ST-elevation acute myocardial infarction than those with the non ST-elevation acute myocardial infarction patients(P<0.05). An increased number of CD4~+CD28~-CX3CR1+T cells was found in the patients with coronary artery disease patients than the control group especially in the ST-elevation acute myocardial infarction patient(P<0.05). Conclusion: CX3CL1 might be involved in the formation of coronary atherosclerotic plaque and played an important role in the atherosclerotic procession,which might be useful to predict the stability of plaque in the early stage of coronary artery disease. [ABSTRACT FROM AUTHOR]

Objective: To study the expressions of chemokine CCL2 in the plasma and the platelets of patients with STEMI, and investigate the effect of CCL2 on P65 and IκBα of the platelets. Methods: 50 patients with STEMI who were admitted in the CCU of General Hospital of Shenyang Military Region from October 2015 to January 2016 and 50 healthy controls were enrolled. The plasma CCL2 concentration of patients with STEMI and healthy controls were detected by ELISA. The expressions of CCL2 and CCR2 in the platelets were detected by western blot; the phosphorylation of P65 and IκBα in the platelets were tested by western blot after CCL2 stimulation, or while CCR2 antagonist RS201895 and NF-κB signaling pathway inhibitor Bayl 1-7082 were pretreated on the platelets. Results: The plasma CCL2 concentration of STEMI patients and healthy controls were 222± 98 pg/mL and 162± 24 pg/mL, there were significant statistical differences between the two groups (P＜0.01). Compared with control group, the expression of CCL2 and CCR2 in the platelets were significantly increased in STEMI patients (P＜0.01). After the platelets were stimulated by CCL2, pP65 increased and IκBα decreased (P＜0.01); when RS201895 or Bay 11-7082 treated before CCL2 stimulation, the phosphorylation of P65 decreased and IκBα increased (P＜0.01). Conclusions: The expression of CCL2 in plasma and platelets of patients with STEMI increased. CCL2/CCR2 might affect the functions of platelets through NF-κB signaling pathway and participate in the thrombosis. [ABSTRACT FROM AUTHOR]

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the association between the ACE gene ID variant with coronary artery disease (CAD) in Northern Han population of China. Methods: In this study we used the gene directing sequencing analysis to detect the ACE gene I/D variant among the 56S CAD patients and 529 control subjects by a case-control study. Results: hi CAD patients and controls subjects, we found that ACE gene ID variant conformed to the Hardy-Weinberg equilibrium well. ACE gene ID variant (II. ID and DD(genotype frequency was 50.3 %. 30.2 % and 19.5 % in CAD patients and 41.7 %. 47.2 % and 11.1 % in controls subjects. ACE gene ID variant maybe a genetic risk factor for CAD in Chinese Han population (P< 0.05). Logistic regression analysis with adjustments for the other risk factors of CAD showed that ACE gene I/D variant significantly increased the risk of CAD compared with the non-carriers (P<0.05). Conclusions: hi Northern Han population of China. ACE gene ID variant maybe considered a genetic risk factor for CAD. [ABSTRACT FROM AUTHOR]

Objective: To investigate the association between the interleukin 23 Receptor (IL23R) rs6682925 variant with coronary artery disease (CAD) in Northern Han population of China. Methods: The study was conducted in 568 coronary artery disease patients and 529 control subjects in a case-control study. We used the gene directing sequencing technology to detect the IL23R rs6682925 and rs1884444 variant. Results: We found that the IL23R rs6682925 and rs1884444 variant frequency conformed well to the Hardy-Weinberg equilibrium in both case and control subject. IL23R rs6682925 (CC, TC and TT) genotype frequency was 22.9 %, 39.6 % and 37.5 % in CAD group and 41.7 %, 47.2 % and 11.1 % in control group. IL23 R rs6682925 C allele was a genetic risk factor for coronary artery disease in Northern Han population of China (P<0.05). There were no significant differences in the genotype and allele distribution of IL23R rs1884444 variant between CAD and control subjects (P>0.05). Logistic regression analysis with adjustments for the other risk factors showed that the C allele carriers of IL23R rs6682925 variant significantly increased the risk of coronary artery disease compared with the non-carriers (P<0.05). Conclusions: IL23R rs6682925 variant may be considered a genetic risk factor for CAD in Northern Han population of China. [ABSTRACT FROM AUTHOR]