Poor correlation between microimmunofluorescence serology and polymerase chain reaction for detection of vascular Chlamydia pneumoniae infection in coronary artery disease patients

1998 ◽  
Vol 187 (2) ◽  
pp. 103-106 ◽  
Author(s):  
M. Maass ◽  
Jens Gieffers ◽  
Eike Krause ◽  
Peter M. Engel ◽  
Claus Bartels ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Polymerase Chain Reaction ◽  
Coronary Artery ◽  
Chlamydia Pneumoniae ◽  
Poor Correlation ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Artery Disease

Periodontal Microbiota in Patients With Coronary Artery Disease Measured by Real-Time Polymerase Chain Reaction: A Case-Control Study

2007 ◽  
Vol 78 (9) ◽  
pp. 1724-1730 ◽  
Author(s):  
Claudia Nonnenmacher ◽  
Michael Stelzel ◽  
Cristiano Susin ◽  
Alexander M. Sattler ◽  
Juergen R. Schaefer ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Polymerase Chain Reaction ◽  
Coronary Artery ◽  
Real Time ◽  
Case Control Study ◽  
Case Control ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Artery Disease ◽  
Control Study

scholarly journals Plasma miR-10a: A Potential Biomarker for Coronary Artery Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Liyun Luo ◽  
Bairong Chen ◽  
Songbiao Li ◽  
Xiaoliang Wei ◽  
Tianmin Liu ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Angina Pectoris ◽  
Lower Plasma ◽  
Chain Reaction ◽  
Qrt Pcr ◽  
Potential Biomarker ◽  
St Elevation ◽  
Polymerase Chain ◽  
Artery Disease

Aims. MicroRNAs (miRNAs) are involved in the pathogenesis of coronary artery disease (CAD). The objective of this study is to determine plasma levels of miR-10a in CAD and analyze its association with the severity of CAD.Materials and Methods. Plasma miR-10a levels in 60 CAD patients including stable angina pectoris (SAP) (n=29), unstable angina pectoris (UAP) or non-ST elevation myocardial infarction (MI) (NSTEMI) (n=17), or ST elevation MI (STEMI) (n=14) and 20 non-CAD subjects were assessed by real-time polymerase chain reaction (qRT-PCR), and associations of miR-10a levels with risk factors of CAD and its severity were analyzed.Results. The qRT-PCR results showed that plasma miR-10a levels were decreased in CAD patients, and CAD with high SYNTAX scores or STEMI was significantly associated with lower miR-10a levels.Conclusions. Lower plasma miR-10a levels were negatively associated with the presence as well as severity of CAD, and plasma miR-10a can act as a potential biomarker for estimating the presence and severity of CAD.

scholarly journals Associations of Galectin-3 Expression and LGALS-3 (rs4652) Gene Variation with Coronary Artery Disease Risk in Diabetics

2021 ◽  
Author(s):  
Samy Hassan ◽  
Mohamed Hassaan ◽  
Basma Demasy ◽  
Norhan Sabbah
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Disease Risk ◽  
Coronary Artery Disease Risk ◽  
Chain Reaction ◽  
Expression Levels ◽  
Gene Variation ◽  
Galectin 3 ◽  
Polymerase Chain ◽  
Artery Disease

Background Galectin‑3 protein that is encoded by lectin galactoside-binding soluble-3 (LGALS-3) gene serves as an important genetic factor in type 2 diabetes mellitus (T2DM) and its cardiovascular obstacles in various populations. We aimed to elicit the pro-inflammatory effect of galectin-3 as determined by interleukin-6 (IL-6) serum levels and to explore the relationship between galectin-3 (LGALS-3 rs4652) gene variation and its expression levels with coronary artery disease (CAD) risk among T2DM Egyptian patients. Methods:  112 lean subjects were compared to 100 T2DM without CAD and 84 T2DM with CAD. A tetra-primer amplification refractory mutation system polymerase chain reaction was used to test LGALS-3 (rs4652) and galectin-3 expression was tested with a quantitative real-time polymerase chain reaction. Serum IL-6 was measured using an enzyme-linked immunosorbent assay. Results: We found that the prevalence of LGALS-3 (rs4652) AC genotype and galectin-3 gene expression levels in T2DM with CAD were significantly higher than the additional 2 groups and were correlated positively to IL-6 circulating levels also, the C allele carriers (AC+CC) had significantly higher relative Galectin-3 expression levels compared to the A allele carriers (AA). Conclusion:  We concluded that galectin-3 expression levels and LGALS-3 (rs4652) AC genotype were coronary artery disease risk factors in type two diabetics among an Egyptian sample.

scholarly journals Relationship between Expression of Plasma lncRNA-HEIH and Prognosis in Patients with Coronary Artery Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Zhenying Zhang ◽  
Sushuang Nan ◽  
Xiujuan Duan ◽  
Lizhong Wang ◽  
Xiaojing Sun ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Adverse Events ◽  
Noncoding Rna ◽  
Quantitative Polymerase Chain Reaction ◽  
Control Group ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Artery Disease ◽  
Cardiac Adverse Events

Objective. We aimed to investigate the expression of long noncoding RNA- (lncRNA-) HEIH in patients with coronary artery disease (CAD) and its impact on patients’ prognosis. Patients and Methods. From July 2015 to December 2018, 250 patients who underwent coronary angiography, including 50 in the control group and 150 in the CAD group, were collected for detection of the expression of lncRNA-HEIH by real-time quantitative polymerase chain reaction (qPCR). The severity of CAD was evaluated through SYNTAX scoring system. In addition, these patients with CAD were followed up for 3 years, and the major cardiac adverse events such as myocardial infarction and revascularization were recorded. Results. The expression of lncRNA-HEIH in plasma of patients with CAD was remarkably higher than that in the control subjects and was verified to be relevant to the severity of CAD. Meanwhile, it was found that CAD patients with high expression of lncRNA-HEIH had higher rates of dyslipidemia as well as CAD family history and higher overall incidence of major cardiac adverse events than those with low expression of lncRNA-HEIH. Conclusions. lncRNA-HEIH expression is upregulated in the plasma of CAD patients, which is capable of affecting the prognosis of patients.

scholarly journals Perivascular Adipose Tissue Inflammation in Ischemic Heart Disease

2021 ◽  
Vol 41 (3) ◽  
pp. 1239-1250
Author(s):  
Celestina Mazzotta ◽  
Sanchita Basu ◽  
Adam C. Gower ◽  
Shakun Karki ◽  
Melissa G. Farb ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Coronary Artery ◽  
Quantitative Polymerase Chain Reaction ◽  
Artery Bypass ◽  
Bypass Graft ◽  
Artery Bypass Graft ◽  
Chain Reaction ◽  
Perivascular Adipose Tissue ◽  
Polymerase Chain ◽  
Artery Disease

Objective: There is growing recognition that adipose tissue–derived proatherogenic mediators contribute to obesity-related cardiovascular disease. We sought to characterize regional differences in perivascular adipose tissue (PVAT) phenotype in relation to atherosclerosis susceptibility. Approach and Results: We examined thoracic PVAT samples in 34 subjects (body mass index 32±6 kg/m 2 , age 59±11 years) undergoing valvular, aortic, or coronary artery bypass graft surgeries and performed transcriptomic characterization using whole-genome expression profiling and quantitative polymerase chain reaction analyses. We identified a highly inflamed region of PVAT surrounding the human aortic root in close proximity to coronary takeoff and adjoining epicardial fat. In subjects undergoing coronary artery bypass graft, we found 300 genes significantly upregulated (false discovery rate Q <0.1) in paired samples of PVAT surrounding the aortic root compared with nonatherosclerotic left internal mammary artery. Genes encoding proteins mechanistically implicated in atherogenesis were enriched in aortic PVAT consisting of signaling pathways linked to inflammation, WNT (wingless-related integration site) signaling, matrix remodeling, coagulation, and angiogenesis. Overexpression of several proatherogenic transcripts, including IL1β , CCL2 ( MCP-1 ), and IL6 , were confirmed by quantitative polymerase chain reaction and significantly bolstered in coronary artery disease subjects. Angiographic coronary artery disease burden quantified by the Gensini score positively correlated with the expression of inflammatory genes in PVAT. Moreover, periaortic adipose inflammation was markedly higher in obese subjects with striking upregulation (≈8-fold) of IL1β expression compared to nonobese individuals. Conclusions: Proatherogenic mediators that originate from dysfunctional PVAT may contribute to vascular disease mechanisms in human vessels. Moreover, PVAT may adopt detrimental properties under obese conditions that play a key role in the pathophysiology of ischemic heart disease. Graphic Abstract: A graphic abstract is available for this article.

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