Coronary artery disease （CAD） is a multifactorial disease in which inflammation plays a central role. This study aimed to investigate the association of inflammatory markers such as the neutrophil to lymphocyte rat...Coronary artery disease （CAD） is a multifactorial disease in which inflammation plays a central role. This study aimed to investigate the association of inflammatory markers such as the neutrophil to lymphocyte ratio （NLR）, the Global Registry of Acute Coronary Events （GRACE） score with in-hospital mortality of elderly patients with acute myocardial infarction （AMI） in an attempt to explore the prognostic value of these indices for elderly AMI patients. One thousand consecutive CAD patients were divided into two groups based on age 60. The laboratory and clinical characteristics were assessed retrospectively by reviewing the medical records. The NLR and GRACE score were calculated. In the elderly （〉60 years）, patients with non-ST-elevation myocardial infarction （NSTEMI） and ST-elevation myocardial infarction （STEMI） had significantly higher NLR than did those with unstable angina （UA） and stable angina pectoris （SAP） （P〈0.01）. The NLR was considerably elevated in older AMI patients compared with their younger counterparts （〈60 years） （P〈0.05）. In elderly AMI patients, the NLR was considerably higher in the high-risk group than in both the low-risk and mediumrisk groups based on the GRACE score （P〈0.05 and P〈0.01, respectively）, and the NLR was positively correlated with the GRACE score （r=0.322, P〈0.001）. Either the NLR level or the GRACE score was significantly higher in the death group than in the surviving group （P〈0.05）. By curve receiver operator characteristic curve （ROC） analysis, the optimal cut-off levels of 9.41 for NLR and 174 for GRACE score predicted in-hospital death [ROC area under the curve （AUC） 0.771 and 0.787, respectively, P〈0.001]. It was concluded that an elevated NLR is a potential predictor of in-hospital mortality in elderly patients with AMI.展开更多
In this study,the hypothesis that Wnt/β-catenin pathway is involved in the arterial calcification by regulating the osteoprotegerin(OPG)/receptor activator of NF-κB ligand(RANKL)system was tested.Theβ-catenin expre...In this study,the hypothesis that Wnt/β-catenin pathway is involved in the arterial calcification by regulating the osteoprotegerin(OPG)/receptor activator of NF-κB ligand(RANKL)system was tested.Theβ-catenin expression was measured in the warfarin-induced calcified arteries and the osteoblast-like cells differentiating from smooth muscle cells(SMCs)by immunohistochemistry and Western blotting.The Wnt/β-catenin pathway was activated or inhibited by lithium chloride(LiCl)or dickkopf 1(DKK1)in vitro and in vivo.Then the calcification level was determined by von Kossa staining,Ca^2+content assay,and alkaline phosphatase(ALP)activity assay.The expression levels of osteocalcin,OPG and RANKL were detected by Western blotting or real-time PCR.The results showed that in calcified arteries and OBL cells,the activation of Wnt/β-catenin pathway significantly enhanced the calcification as evidenced by increased von Kossa stains,Ca^2+contcnts,ALP activities,and osteocalcin expression levels(P<0.05),and it promoted the RANKL expression(P<0.05),but slightly affected the OPG expression.These results indicated that the activation of Wnt/β-catenin pathway worsens the arterial calcification,probably by promoting the RANKL expression.展开更多
Heart failure （HF） is the end stage of various kinds of cardiovascular diseases and leads to a high mortality worldwide. Numerous studies have demonstrated that frequencies of CD4＋CD25＋Foxp3＋ regulatory T cells ...Heart failure （HF） is the end stage of various kinds of cardiovascular diseases and leads to a high mortality worldwide. Numerous studies have demonstrated that frequencies of CD4＋CD25＋Foxp3＋ regulatory T cells （Tregs） are reduced in HF patients and properly expanding Tregs attenuates HF progression. Histone deacetylase （HDAC） 9 has been revealed to contribute to several cardiovascular and cerebrovascular diseases. Plenty of studies showed that HDAC9 negatively regulated the number and function of Tregs. Thus, we aim to investigate the expression of HDAC 9 in patients with chronic heart failure （CHF） and the relationship among HDAC9, Tregs and CHF. Our research showed a reduced number of Tregs and an increased expression of HDAC9 mRNA in CHF patients. Patients with CHF were divided into two groups by heart function grade of New York Heart Association （NYHA）, we found that the HDAC9 mRNA expression level in NYHA grade Ⅱ -Ⅲ group were lower than that in NYHA grade IV group. More importantly, the correlation study suggested that the expression of HDAC9 mRNA was negatively correlated to Tregs frequency and left ventricular ejection fraction （LVEF）, whereas positively correlated to larger left ventricular end-diastolic dimension （LVEDD） and B-type natriuretic peptide （BNP） in patients with CHF. The correlation studies also showed a positive correlation between HDAC9 and the severity of CHF. Our research suggests that HDAC9 may be a new indicator for assessing CHF and it may offer a new direction for research of CHF.展开更多
基金This project was supported by a grant from Hubei Natural Science Foundation of China （No. 2013CKB011）.
文摘Coronary artery disease （CAD） is a multifactorial disease in which inflammation plays a central role. This study aimed to investigate the association of inflammatory markers such as the neutrophil to lymphocyte ratio （NLR）, the Global Registry of Acute Coronary Events （GRACE） score with in-hospital mortality of elderly patients with acute myocardial infarction （AMI） in an attempt to explore the prognostic value of these indices for elderly AMI patients. One thousand consecutive CAD patients were divided into two groups based on age 60. The laboratory and clinical characteristics were assessed retrospectively by reviewing the medical records. The NLR and GRACE score were calculated. In the elderly （〉60 years）, patients with non-ST-elevation myocardial infarction （NSTEMI） and ST-elevation myocardial infarction （STEMI） had significantly higher NLR than did those with unstable angina （UA） and stable angina pectoris （SAP） （P〈0.01）. The NLR was considerably elevated in older AMI patients compared with their younger counterparts （〈60 years） （P〈0.05）. In elderly AMI patients, the NLR was considerably higher in the high-risk group than in both the low-risk and mediumrisk groups based on the GRACE score （P〈0.05 and P〈0.01, respectively）, and the NLR was positively correlated with the GRACE score （r=0.322, P〈0.001）. Either the NLR level or the GRACE score was significantly higher in the death group than in the surviving group （P〈0.05）. By curve receiver operator characteristic curve （ROC） analysis, the optimal cut-off levels of 9.41 for NLR and 174 for GRACE score predicted in-hospital death [ROC area under the curve （AUC） 0.771 and 0.787, respectively, P〈0.001]. It was concluded that an elevated NLR is a potential predictor of in-hospital mortality in elderly patients with AMI.
文摘In this study,the hypothesis that Wnt/β-catenin pathway is involved in the arterial calcification by regulating the osteoprotegerin(OPG)/receptor activator of NF-κB ligand(RANKL)system was tested.Theβ-catenin expression was measured in the warfarin-induced calcified arteries and the osteoblast-like cells differentiating from smooth muscle cells(SMCs)by immunohistochemistry and Western blotting.The Wnt/β-catenin pathway was activated or inhibited by lithium chloride(LiCl)or dickkopf 1(DKK1)in vitro and in vivo.Then the calcification level was determined by von Kossa staining,Ca^2+content assay,and alkaline phosphatase(ALP)activity assay.The expression levels of osteocalcin,OPG and RANKL were detected by Western blotting or real-time PCR.The results showed that in calcified arteries and OBL cells,the activation of Wnt/β-catenin pathway significantly enhanced the calcification as evidenced by increased von Kossa stains,Ca^2+contcnts,ALP activities,and osteocalcin expression levels(P<0.05),and it promoted the RANKL expression(P<0.05),but slightly affected the OPG expression.These results indicated that the activation of Wnt/β-catenin pathway worsens the arterial calcification,probably by promoting the RANKL expression.
文摘Heart failure （HF） is the end stage of various kinds of cardiovascular diseases and leads to a high mortality worldwide. Numerous studies have demonstrated that frequencies of CD4＋CD25＋Foxp3＋ regulatory T cells （Tregs） are reduced in HF patients and properly expanding Tregs attenuates HF progression. Histone deacetylase （HDAC） 9 has been revealed to contribute to several cardiovascular and cerebrovascular diseases. Plenty of studies showed that HDAC9 negatively regulated the number and function of Tregs. Thus, we aim to investigate the expression of HDAC 9 in patients with chronic heart failure （CHF） and the relationship among HDAC9, Tregs and CHF. Our research showed a reduced number of Tregs and an increased expression of HDAC9 mRNA in CHF patients. Patients with CHF were divided into two groups by heart function grade of New York Heart Association （NYHA）, we found that the HDAC9 mRNA expression level in NYHA grade Ⅱ -Ⅲ group were lower than that in NYHA grade IV group. More importantly, the correlation study suggested that the expression of HDAC9 mRNA was negatively correlated to Tregs frequency and left ventricular ejection fraction （LVEF）, whereas positively correlated to larger left ventricular end-diastolic dimension （LVEDD） and B-type natriuretic peptide （BNP） in patients with CHF. The correlation studies also showed a positive correlation between HDAC9 and the severity of CHF. Our research suggests that HDAC9 may be a new indicator for assessing CHF and it may offer a new direction for research of CHF.
