Bile acid synthesis precursors in subjects with genetic hypercholesterolemia negative for LDLR/APOB/PCSK9/APOE mutations. Association with lipids and carotid atherosclerosis.
The ApoE4 genotype may be a risk factor for carotid atherosclerosis, but is not correlated with bone mineral density (BMD) in the lumbar spine in elderly Han males.
Nuclear magnetic resonance lipoprotein subclasses and the APOE genotype influence carotid atherosclerosis in patients with systemic lupus erythematosus.
Additionally, study subjects with two risk genotypes of APOE and MCP-1 and either had ingested well water contained arsenic level >10 microg/L or had arsenic exposure >0.22 mg/L-year would have strikingly highest risk of 10.3-fold and 15.7-fold, respectively, for the development carotid atherosclerosis, showing significant joint effect of arsenic exposure and risk genotypes of APOE and MCP-1.
Additionally, study subjects with two risk genotypes of APOE and MCP-1 and either had ingested well water contained arsenic level >10 microg/L or had arsenic exposure >0.22 mg/L-year would have strikingly highest risk of 10.3-fold and 15.7-fold, respectively, for the development carotid atherosclerosis, showing significant joint effect of arsenic exposure and risk genotypes of APOE and MCP-1.
This cross-sectional study showed a synergistic effect between the intron 4 polymorphism or T(-786)-->C polymorphism of the eNOS gene and the apoE polymorphism with respect to risk for carotid atherosclerosis in nondiabetic hemodialysis patients.
We investigated the distribution of four genetic polymorphisms (angiotensin converting enzyme [ACE], methylenetetrahydrofolate reductase [MTHFR], apolipoprotein E [apo E], and paraoxonase [PON] genes) in 30 subjects with VaSA, 30 subjects with moderate carotid atherosclerosis (ATS group), and 161 controls with a negative history for cardiovascular disease.
Twenty-seven young (<50 years old) patients with spontaneous carotid artery dissection in 11 cases and carotid atherosclerosis in 16 cases were evaluated to determine the apolipoprotein E polymorphism.
Our data suggested a synergistic effect between the apoE allele epsilon(4) and smoking on carotid atherosclerosis: odds ratios were 1.7 (95% CI, 0.8 to 3.6) for smoking alone, 1.0 (95% CI, 0.6 to 1.8) for epsilon4 alone, and 3.7 (95% CI, 1.1 to 3.6) for the joint presence of the apoE allele epsilon4 and smoking.
Our data confirm the influence of apoE4 on cholesterol levels and clearly show that apoE genotype affects carotid atherosclerosis in its early stages in middle-aged asymptomatic subjects.
We evaluated the associations of 10 biomarkers of systemic inflammation (CRP, IL-6, sTNF-αR1 and 2), monocyte activation (CCL2, sCD163, sCD14), coagulation (fibrinogen, D-dimer), and endothelial dysfunction (ICAM-1) with subclinical carotid atherosclerosis among participants in the Multicenter AIDS Cohort Study (MACS).
The -928 guanine (G)/cytosine (C) and -362 G/C single-nucleotide polymorphisms (SNPs) in the proximal promoter region of the monocyte chemoattractant protein 1 gene have been associated with an increased risk for intimal medial thickness and carotid atherosclerosis, respectively.
The objective of this study was to evaluate the relation between the genotypes of the MCP-1A-2518G polymorphism and the development of carotid atherosclerosis in patients with type 2 diabetes.
Single nucleotide polymorphisms in monocyte chemoattractant protein-1 and its receptor act synergistically to increase the risk of carotid atherosclerosis.
Additionally, study subjects with two risk genotypes of APOE and MCP-1 and either had ingested well water contained arsenic level >10 microg/L or had arsenic exposure >0.22 mg/L-year would have strikingly highest risk of 10.3-fold and 15.7-fold, respectively, for the development carotid atherosclerosis, showing significant joint effect of arsenic exposure and risk genotypes of APOE and MCP-1.
Additionally, study subjects with two risk genotypes of APOE and MCP-1 and either had ingested well water contained arsenic level >10 microg/L or had arsenic exposure >0.22 mg/L-year would have strikingly highest risk of 10.3-fold and 15.7-fold, respectively, for the development carotid atherosclerosis, showing significant joint effect of arsenic exposure and risk genotypes of APOE and MCP-1.
The purpose of this study was to clarify the association of the plasma level of MCP-1 and the SNP of the MCP-1 gene with carotid atherosclerosis in community-based subjects.