Correlation Of Apolipoprotein Research Articles

Correlation of Apolipoprotein a-i with Renal Function in Diabetic Patients

Correlation of Apolipoprotein a-i with Renal Function in Diabetic Patients

The Correlation of Apolipoprotein B with Alterations in Specific Fat Depots Content in Adults.

Body mass index (BMI) and blood biomarkers are not enough to predict cardiovascular disease risk. Apolipoprotein B was identified to be associated with cardiovascular disease (CVD) progression. The Dual-energy X-ray Absorption (DXA) results could be considered as a predictor for cardiovascular disease in a more refined way based on fat distribution. The prediction of CVD risk by simple indicators still cannot meet clinical needs. The association of ApoB with specific fat depot features remains to be explored to better co-predict cardiovascular disease risk. An amount of 5997 adults from National Health and Nutrition Examination Survey (NHANES) were enrolled. Their demographic information, baseline clinical condition, blood examination, and DXA physical examination data were collected. Multivariate regression was used to assess the correlation between ApoB and site-specific fat characteristics through different adjusted models. Smooth curve fittings and threshold analysis were used to discover the turning points with 95% confidence intervals. ApoB is positively correlated with arms percent fat, legs percent fat, trunk percent fat, android percent fat, gynoid percent fat, arm circumference and waist circumference after adjustment with covariates for age, gender, race, hypertension, diabetes, hyperlipidemia, coronary heart disease, smoking status and vigorous work activity. The smooth curve fitting and threshold analysis also showed that depot-specific fat had lower turning points of ApoB in both males and females within the normal reference range of ApoB. Meanwhile, females have a lower increase in ApoB per 1% total percent fat and android percent fat than males before the turning points, while females have a higher growth of ApoB per 1% gynoid percent fat than males. The combined specific fat-depot DXA and ApoB analysis could indicate the risk of CVD in advance of lipid biomarkers or DXA alone.

Correlation of apolipoprotein A-I with T cell subsets and interferon-ү in coronary artery disease.

The association of Apolipoprotein A-I (APOAI) with T cell subsets and interferon-ү (IFN-γ) in patients with coronary artery disease (CAD) has been not reported. Thus, this study aimed to investigate the association of APOAI with T cell subsets and IFN-γ in CAD. This study included a total of 107 patients with CAD including acute coronary syndrome and chronic coronary syndrome. T cell subsets, and CD3-CD56+ natural killer cells were quantified by flow cytometric analysis. The serum concentrations of IFN-ү were measured by enzyme-linked immunosorbent assay. Lipid profiles, C-reactive protein (CRP), and fibrinogen were measured in the clinical laboratory. Clinical data was obtained duration hospitalization. The CD4+ T cells were higher in patients of the low-APOAI group (<median: 1.2 mmol/L) than in patients of the high-APOAI group(≥median: 1.2 mmol/L) (p < .05). The CD8+ T cells were lower in patients of the low APOAI group than in patients of the high-APOAI group (p < .05). APOAI was inversely associated with CD4+ T cells, IFN-γ, and was positively associated with CD8+ T cells (p < .05). No correlation was observed between CD3 + CD56+ cells, regulatory T cells (Tregs), and CD3-CD56+ natural killer cells and APOAI (p > .05). The high-density lipoprotein cholesterol (HDL-C) was also inversely associated with CD4+ T cells (p < .05), and positively associated with CD8+ T cells (p < .05). Lastly, APOA1 and HDL-C did not correlated with fibrinogen and CRP (p > .05). The present study demonstrated the correlation of APOAI with T cell subsets and IFN-γ in CAD. These results provided novel information for the regulatory action between APOAI and T cell subsets and inflammatory immunity in CAD.

Correlation of Apolipoprotein B mRNA-editing Enzyme, Catalytic Polypeptide- like 3G Genetic Variant rs8177832 with HIV-1 Predisposition in Pakistani Population.

Background: Human immunodeficiency virus (HIV) infection is a global health burden which ultimately results in acquired immune deficiency syndrome (AIDS). There are multiple host fac-tors which are capable of limiting HIV-1 replication. One of the most important host factors which in-hibit HIV-1 DNA synthesis is the apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G (APOBEC3G). Any genetic variation of this important host factor may influence the host suscep-tibility to viral infection.Objective: The aim of the current study was to evaluate any correlation of APOBEC3G genetic varia-tion rs8177832 with HIV-1 infection.Methods: The study involved 142 healthy control and 100 HIV-1 infected subjects. The genetic varia-tion rs8177832 of all studied subjects was determined by allele-specific polymerase chain reaction (AS-PCR).Results: The results showed that the distribution of rs8177832 genotypes AA, AG and GG in healthy subjects and HIV-1 subjects was; 42.253%, 42.957%, 14.788% and 66%, 27%, 7% respectively. Sta-tistical analyses of data showed that there was a significant variation in rs8177832 genotype AA in healthy control and HIV-1 infected subjects (42.257% vs 66%; p-value<0.001).Conclusion: Thus it was concluded that APOBEC3G rs8177832 AA genotype contributes in genetic predisposition to HIV-1 infection in Pakistani population.

Correlation of apolipoprotein A-I kinetics with survival and response to first-line platinum-based chemotherapy in advanced non-small cell lung cancer.

The aim of this study was to determine whether apolipoprotein A-I (ApoA-I) kinetics predict the overall survival in patients with advanced-stage non-small cell lung cancer (NSCLC) during platinum-based first-line therapy. A total of 125 NSCLC patients from January 2008 to September 2014 were retrospectively reviewed. Serum ApoA-I level was measured at baseline and thereafter at the start of each palliative chemotherapy cycle for all patients. Patients were divided into four groups according to ApoA-I kinetics. Patients whose ApoA-I≥1.01g/L and never decreased during treatment, patients whose ApoA-I≥1.01g/L and decreased (ApoA-I<1.01g/L) at least one time during treatment, patients whose ApoA-I<1.01g/L and normalized (ApoA-I≥1.01) at least one time during treatment, and patients whose ApoA-I<1.01g/L and never normalized during treatment were assigned to non-decreased, decreased, normalized, and non-normalized ApoA-I groups, respectively. Overall survival rates were significantly different between the four groups, with 2-year survival rates of 88.6 and 17.5% for the non-decreased and the decreased ApoA-I groups, respectively, and none survived 2years later in the normalized and the non-normalized ApoA-I groups. When compared with the non-decreased group, the hazard ratios of death were 0.05, 0.44, and 1.73 in the normalized, decreased, and non-normalized groups, respectively (P<0.001). Normalization of ApoA-I was associated with a low risk of progression, whereas patients with a decreased level of ApoA-I showed a progression of disease in most cases. ApoA-I can be a novel, widely available biomarker for patients with NSCLC.

Non–high-density lipoprotein cholesterol is associated more closely with albuminuria in Chinese type 2 diabetic patients with normal renal function, compared with traditional lipid parameters

Urinary albumin excretion rate (UAER) is a remarkable index reflecting the progression of kidney disease in diabetic subjects. The link between UAER and lipid metabolism is still unclear. The correlation of Apolipoprotein B (ApoB) to albuminuria has been investigated. The National Cholesterol Education Program-Adult Treatment Panel III recommends that clinicians consider non-high-density lipoprotein cholesterol (non-HDL-c) as a surrogate marker for ApoB. We sought to evaluate the relationship of UAER with lipid profile, especially with non-HDL-c in type 2 diabetic patients without renal dysfunction. A total of 507 type 2 diabetic patients with normal renal function participated in this study. Demographic and anthropometric data were collected; 24-hour urine samples were collected for UAER measurement. Blood samples were collected for lipid parameters and HbA1c measurement. The patients with albuminuria had greater levels of non-HDL-c and ApoB. The frequencies of albuminuria among the four quartiles of lipid parameters, ie, triglycerides, total cholesterol, non-HDL-c, and ApoB, demonstrated significantly linearly increasing (P for trend <.01). After adjustment, UAER was significantly correlated with total cholesterol, triglycerides, ApoB, and non-HDL-c but not with low-density lipoprotein cholesterol (LDL-c) or lipoprotein(a) [Lp(a)]. Stepwise regression analysis showed that age (β= .255, P= .000), systolic blood pressure (β= .261, P= .000), non-HDL-c (β= .164, P= .000), and duration of diabetes (β= .105, P= .024) were independently correlated with UAER in diabetic patients without renal dysfunction. Compared with the lipid parameters of total cholesterol, triglycerides, HDL-c, LDL-c, ApoB, Apolipoprotein A-I (ApoA-I), and Lp(a), non-HDL-c was more closely associated with albuminuria in Chinese type 2 diabetic patients without impaired renal function.

Diagnosis and Biochemical Mechanisms of Multiple Forms of Alzheimer's Disease Based on the Correlation of Apolipoprotein E Isoforms with the Differences in Serum Concentration of 45 Additional Protein Biomarkers

Diagnosis and Biochemical Mechanisms of Multiple Forms of Alzheimer's Disease Based on the Correlation of Apolipoprotein E Isoforms with the Differences in Serum Concentration of 45 Additional Protein Biomarkers

Diagnosis and biochemical mechanisms of multiple forms of Alzheimer's disease based on the correlation of Apolipoprotein E isoforms with the differences in serum concentration of 45 additional protein biomarkers

Diagnosis and biochemical mechanisms of multiple forms of Alzheimer's disease based on the correlation of Apolipoprotein E isoforms with the differences in serum concentration of 45 additional protein biomarkers

FP49-TH-05 Correlation of apolipoprotein E polymorphism and age of onset in Javanese with vascular dementia in Yogyakarta

FP49-TH-05 Correlation of apolipoprotein E polymorphism and age of onset in Javanese with vascular dementia in Yogyakarta

The correlation of apolipoprotein B, apolipoprotein B/apolipoprotein A-I ratio and lipoprotein(a) with myocardial infarction

Abstract Recent evidence shows that apolipoprotein (apo) B, apoB/apoA-I ratio and lipoprotein(a) are better indicators of coronary risk than the conventional lipid profile. The aim of this study was to evaluate the correlation of apoA-I and B, and lipoprotein(a) with myocardial infarction (MI). We performed a cross-sectional study including 208 patients (100 men and 108 women), with and without previous MI evaluated by coronary angiography. The severity of coronary heart disease was scored on the basis of the number and extent of lesions in the coronary arteries. Lipid levels were measured by the enzymatic method and apolipoprotein levels were measured by the immunoturbidimetric method. The MI group had higher plasmatic levels of lipoprotein(a) (0.37±0.28 vs. 0.29±0.23 g/L, p&lt;0.05), apoB (1.13±0.40 vs. 0.84±0.28 g/L, p&lt;0.05) and of the apoB/apoA-I ratio (0.77±0.37 vs. 0.68±0.20, p&lt;0.05) compared to controls. The area under the receiver operating characteristic (ROC) curves (AUC) suggested a good reliability in the diagnose of coronary heart disease for the apoB/apoA-I ratio (0.756, p&lt;0.05), apoB (0.664, p&lt;0.05), lipoprotein(a) (0.652, p&lt;0.05) and total cholesterol/HDL-cholesterol (0.688, p&lt;0.05). Multivariate analysis performed with adjustments for cardiovascular risk factors, showed that the levels of lipoprotein(a), apoB and apoB/apoA-I ratio are significant independent cardiovascular risk factors. Our results indicate that there is an important relationship among high plasma apoB concentration, lipoprotein(a) concentration, the apoB/apoA-I ratio, and MI. We showed that the apoB/apoA-I ratio has a stronger correlation with MI than the total cholesterol/HDL cholesterol ratio. We therefore suggest using apoB/apoA-I ratio and lipoprotein(a) in clinical practice as a markers of MI risk.

Correlation of apolipoprotein M with leptin and cholesterol in normal and obese subjects

Apolipoprotein M (apoM) is a recently characterized apolipoprotein that is exclusively expressed in the liver and kidney. In plasma it is present predominantly in high-density lipoprotein (HDL). The physiological function of apoM is not yet known. In the present study we investigated relationships between plasma apoM levels and leptin levels, body mass index (BMI), as well as fasting glucose and other lipid parameters in women with a wide range of BMI (18.9–57.1 kg/m 2, n = 51). In univariate analysis, apoM correlated significantly with leptin ( r = 0.54, P < 0.001), BMI ( r = 0,70, P < 0.001), fasting insulin ( r = 0.33, P = 0.025), total cholesterol ( r = −0.41, P = 0.016), and LDL-cholesterol ( r = −0.39, P = 0.018). The correlations between apoM and cholesterol and between apoM and leptin remained significant after adjustment for the influence of BMI. Forward stepwise multiple regressions when leptin, BMI, insulin, and cholesterol were entered into a model as independent variables and apoM as the dependent variable, showed that cholesterol and leptin were independent predictors of circulating apoM. These two parameters yielded a value of r 2 = 0.28, thereby explaining approximately 30% of the variance in apoM. Hence, we show that apoM is positively related to leptin and negatively related to cholesterol in humans.

Correlation of apolipoprotein(a) isoproteins with Lp(a) density and distribution in fasting plasma

Lp(a) is an LDL-like lipoprotein which contains an additional apolipoprotein called apo(a). Apo(a) exhibits s significant size polymorphism and its size is inversely correlated with plasma Lp(a) levels. We investigated the distribution of different apo(a) isoproteins in lipoprotein density fractions. Fasting plasma samples were subjected to non-equilibrium density gradient ultracentrifugation. After SDS-PAGE and anti-apo(a) immunoblotting, apo(a) concentrations in individual density fractions were evaluated by densitometry. In series I, analysis of selected density fractions from 35 coronary heart disease (CHD) patients demonstrated that although most of the apo(a) was present in the Lp(a) density range, apo(a) was consistently found in both the VLDL and IDL fractions as well. In series II, density fractions from 9 normolipidemic subjects with 6 different apo(a) isoproteins were evaluated. A strong association between the size of the apo(a) isoprotein and the density of the associated Lp(a) particle was established ( r = 0.976, P < 0.001). Lp(a) densities ranged from 1.057 g/ml for the B isoprotein to 1.09 g/ml for the S5 isoprotein. Overall, 75% of the total apo(a) was detected in the Lp(a) density range ( d = 1.05–1.12 g/ml), with 9% and 10% in the LDL ( d = 1.019–1.05 g/ml) and HDL ( d = 1.12–1.21 g/ml) fractions, respectively. VLDL contained an average of 4% of the total apo(a) in fasting normolipidemic plasma. Two hypertriglyceridemic subjects had substantially greater amounts of apo(a) in the fasting triglyceride-rich fraction. The results of this study indicate that the size of the apo(a) isoprotein strongly influences the density of its associated Lp(a) particle and that apo(a) is consistently found in the triglyceride-rich lipoproteins of fasting plasma.