Objectives: Cardiovascular diseases (CVDs) are responsible of 31% of all deaths worldwide. Genetic predisposition to CVDs in adolescents remains largely unknown. Aims of present research are to examine the association of ADIPOQ gene polymorphisms with cardiovascular disease risk factors in European adolescents.

Methods: A total of 14 polymorphisms in the ADIPOQ gene were genotyped in 1057 European adolescents (12-18 years old) from the Healthy Lifestyle in Europe by Nutrition in Adolescence Cross-Sectional Study. We measured serum lipids and a CVD risk score, along with weight, height, triceps, and subscapular skinfold thickness, leptin, insulin and other markers of glucose regulation.

Results: The rs822393, rs822395 and rs7649121 polymorphisms of ADIPOQ gene were significantly associated with several CVD risk factors [i.e. high-density lipoprotein cholesterol (HDL-C), apolipoprotein (Apo) A1, SBP and CVD risk score] in European adolescents. We also found an association of the TGAAGT ADIPOQ haplotype (rs822393, rs16861210, rs822395, rs822396, rs12495941 and rs7649121) with HDL-C and ApoA1 levels.

Conclusion: Several individual polymorphisms (rs822393, rs822395 and rs7649121) and a haplotype of ADIPOQ gene were significantly associated with cardiovascular disease risk factors in European adolescents.

Apolipoproteins (Apo) are known atherogenic factors that play important roles in many mechanisms related to coronary heart disease. The ApoB/ApoA1 ratio is a promising diagnostic tool for metabolic syndrome (MS) in different populations, though its use is not established in Kazakhstan. This study aimed to assess the relationship between MS and the ApoB/ApoA1 ratio among hypertensive patients and to evaluate its diagnostic use for identifying MS as an alternative to triglycerides (TG) and high-density lipoprotein cholesterol (HDL-C). A cross-sectional study was conducted in 800 eligible men and women with primary hypertension from April 2015 to December 2016. Data were collected on socio-demographics, lifestyle parameters, family history of cardiovascular disease, and hypertension. Dietary Quality Score (DQS), anthropometric data, and blood pressure were recorded; ApoA1 and ApoB levels were measured in blood samples. We found a significant positive association between MS and the ApoB/ApoA1 ratio by multiple logistic regression, as shown by a linear trend of increase of the odds ratio (OR) for MS across the quartiles of ApoB/ApoA1 (p < 0.0001). ROC analysis revealed diagnostic significance of the ApoB/ApoA1 ratio for MS, and comparative ROC analysis demonstrated equal diagnostic value of ApoB/ApoA1 ratio and TG levels (AUC = 0.71 (95% CI 0.69; 0.74) and 0.72 (95% CI 0.69, 0.76), respectively), which was significantly higher than those of HDL, ApoA1, ApoB (AUC = 0.27 (95% CI 0.23; 0.31), AUC = 0.37 (95% CI 0.33; 0.41), AUC = 0.67, (95% CI 0.63; 0.71), respectively). The diagnostic value of the ApoB/ApoA1 ratio in Kazakhs with MS appeared to equal that of TG and was significantly higher than that of HDL-C. Adjusting for gender, smoking, and DQS significantly strengthened the association between MS and the ApoB/ApoA1 ratio in the Kazakh population.

Keywords: Kazakhstan; apolipoprotein A1; apolipoprotein B; cardiovascular diseases; high-density lipoprotein cholesterol (HDL-C); hypertension; metabolic syndrome; multiple regression; smoking; triglycerides.

Current studies suggest a derangement of the cholesterol homeostasis in certain types of leukaemia. The low serum cholesterol levels observed in patients with AML have been related to the tumoral mass and to the disease activity. Only a few studies have taken into consideration a possible change of the serum lipids in ALL. The aim of this study was to evaluate a possible prognostic significance of serum levels of total cholesterol (TC), triglycerides, HDL-C, LDL-C, VLDL-C, apolipoproteins A1 and B and lipoprotein (a), investigated in 10 newly diagnosed ALL patients before and after induction treatment. At diagnosis all these parameters were not significantly different in our patients vs control group except cholesterol and HDL-C levels, which were significantly lower. After the induction treatment, we found a significant increase of HDL-C and Apo A1 values only in those patients that achieved a complete remission. These results support the idea that some serum lipids, such as HDL-C and Apo A1, may have a role as early and reliable markers of the effectiveness of chemotherapy.

Several previous studies have shown the benefits of deep sea water (DSW) in lipid metabolism. However, the effects of DSW on cellular cholesterol accumulation and synthesis induced by high glucose or free fatty acid plus high glucose [4.5g/L] (FFA/glucose) have not been fully elucidated to date. Herein, we showed the effects of mineral-balanced DSW [magnesium (Mg):calcium (Ca)=3:1] (MB-DSW) on cholesterol metabolism induced by high glucose or FFA/glucose in HepG2 hepatic cells. Moreover, the effects of high ratio Mg DSW [Mg:Ca=40:1] (Mg40) were also investigated. MB-DSW and Mg40 prevented the increase of cellular total cholesterol content in high glucose- or FFA/glucose-treated HepG2 hepatic cells. Furthermore, the inhibition by MB-DSW was closely related to the down-regulation of 3-hydroxy-3-methylglutatryl-CoA reductase (HMGCR) expression and an increase in the AMP-activated protein kinase (AMPK) phosphorylation, leading to decreased cholesterol synthesis in both high glucose- and FFA/glucose-treated conditions. However, this effect was not seen in case of Mg40. In addition, both MB-DSW and Mg40 induced the low-density lipoprotein receptor (LDLR) and diminished the proprotein convertase subtilisin/kexin type 9 (PCSK9) transcriptions in high glucose-treated HepG2 hepatic cells. This result demonstrates that the hypocholesterolemic effects of MB-DSW and Mg40 are mediated with LDL-c clearance through increases of LDLR and its transcription factors, such as peroxisome proliferator-activated receptor-α (PPAR-α), sterol regulatory element-binding protein (SREBP)-1a, and SREBP-2, mRNA synthesis and suppression of PCSK9 transcription. Moreover, apolipoprotein (Apo) A1 transcription was enhanced by MB-DSW and Mg40 without decreasing the expression of Apo B in high glucose-treated HepG2 hepatic cells. However, ApoA1 protein expression was not changed. Taken together, the present investigation suggests that DSW may prevent the high glucose- or FFA/glucose-induced increase of cellular cholesterol levels by inducing LDLR and ApoA1 transcriptions and inhibiting PCSK9 mRNA expression in HepG2 hepatic cells. Additionally, the ratio of Mg in DSW is an important factor that determines whether HMGCR expression and/or AMPK phosphorylation participate in the hypocholesterolemic effects of DSW.

Proprotein convertase subtilisin/kexin 9 (PCSK9) plays an important role in lipid metabolism while available literature regarding its involvement in the pathogenesis of atherosclerosis and in the expression of genes associated with apoptosis and inflammation is constantly increasing. Patients with chronic kidney disease (CKD) experience disproportionately increased cardiovascular morbidity and mortality due to dyslipidemia, accelerated atherosclerosis, inflammation, oxidative stress, and other risk factors. In the present cross-sectional study, we investigated the possible association of serum PCSK9 levels with markers of inflammation, oxidative stress, and endothelial damage in patients with CKD. Patients and Methods. Ninety-two patients with CKD stages II-ΙV (eGFR CKD-EPI 47.3 ± 25.7 ml/min/1.73 m², mean age 66 years, 51 men) were included in the study. Plasma PCSK9 levels were correlated with comorbidities (arterial hypertension, diabetes mellitus, and history of cardiovascular disease), renal function indices (eGFR, proteinuria-UPR/24 h), lipid parameters (LDL-cholesterol, HDL-cholesterol, triglycerides, Lp(a), APO-A1, and APO-B), and soluble biomarkers of inflammation, oxidative stress, and endothelial damage (hs-CRP, fibrinogen, 8-epiPGF2a, ox-LDL, IL-6, TNF-α, sICAM-1, and sVCAM-1). Results. The mean plasma value of PCSK9 was 278.1 ng/ml. PCSK9 levels showed direct correlation with serum triglycerides (p = 0.03), Lp(a) (p = 0.01), and sICAM-1 levels (p = 0.03). There was no significant correlation between PCSK9 levels and indices of the renal function, other lipid profile parameters, inflammatory markers, or comorbidities. Multiple regression analysis showed a significant effect of Lp(a) on PCSK9 levels, and for each unit of higher Lp(a), an increase by 3.082 is expected (95% CI: 0.935-5.228, p = 0.006). At the same time, patients receiving statins are expected to have on average 63.8 ng/ml higher PCSK9 values compared to patients not receiving statins (95% CI: 14.6-113.5, p = 0.012). Conclusion. Plasma levels of PCSK9 in nondialysis CKD patients are correlated with endothelial dysfunction and lipid metabolism parameters. Statin intake increases PCSK9 levels significantly in this patient population. PCSK9 levels are not correlated with the severity of kidney disease. Major prospective studies are necessary to investigate the role of PCSK9 in the atherosclerotic cardiovascular outcome in CKD.

Myocyte enhancer factor 2 (MEF2; MEF2A-MEF2D) transcription factors regulate gene expression in a variety of developmental processes by binding to AT-rich DNA motifs via highly conserved N-terminal extensions known as MADS-box and MEF2 domains. Despite the fact that MEF2 proteins exhibit high similarity at their N-terminal regions and share a common consensus DNA binding motif, their functional preferences may vary significantly in the adjacent regions to the DNA binding core segment. The current study delineates the conformational paradigm, clustered recognition, and comparative DNA binding preferences for MEF2A and MEF2B-specific MADS-box/MEF2 domains at the YTA(A/T)4TAR consensus motif. In both MEF2A and MEF2B proteins, α1-helix plays a crucial role through acquiring more flexibility by attaining loop conformation. In comparison to apo-MEF2, an outward disposition of the distal portion of α1-helix and movement of its proximal part to β1 allows synergistic repositioning of the α1-α2 linker, C-terminal region, and MEF2 domain, resulting in the formation of a hydrophobic groove for DNA binding. In both instances, conformational switching of the helical content is the main contributing factor while preserving the overall β-topology to maintain the inside-out conformation of subdivided α1-helix flip. Multivariate statistical analysis reveals that MEF2B obscures less accessible conformational space for DNA binding as compared to the MEF2A-DNA complex. The presence of similar structural requirements and conserved residues including Arg10, Phe21, and Arg24 in accentuating the MEF2-specific DNA recognition mechanism led us to perform structure-based virtual screening for isolating novel inhibitors that are able to target MEF2-DNA binding regions. The top hits (acetamide, benzamide, carboxamide, and enamide) obtained through preliminary assay were scrutinized to binding potential analysis at the MEF2-DNA binding groove, energy values, absorption, distribution, toxicity, and Lipinski's rule of five assessments. Based on these findings, we propose valuable active drug-like molecules for selective applications against MEF2A and MEF2B. The current study may help in uncovering the atomistic-level mechanistic DNA binding patterns of MEF2 proteins, and data may be valuable in devising effective therapeutic strategies for MEF2-associated disorders.

Today, eggs with an increased content of -3 fatty acids are available but there are few publications on the effects of consumption of such eggs on the lipoproteins and acute phase markers in humans. The aim of the present study was to evaluate the effects of consumption of standard eggs and -3 enriched eggs on lipoproteins, glucose and inflammation markers. Nineteen healthy volunteers consumed one extra egg per day of either standard eggs or omega-3 enriched eggs in a double-blind, cross-over study. The duration of each period was 1 month. The effects of the different egg diets on apolipoprotein A1 and B (Apo A1 and B), lipoprotein (a), creatinine, cystatin C, C-reactive protein, serum amyloid protein A, interleukin 6, triglycerides, glucose, total-, high-density lipoprotein and low-density lipo-protein cholesterol concentrations were analyzed. Addition of one regular egg per day to the normal diet had no negative impact on blood lipids or inflammation markers. Consumption of omega-3 enriched eggs resulted in higher levels of ApoA1, lower ApoB/ApoA1 ratio and lower plasma glucose. These effects have been associated in previous studies with a reduced risk for cardiovascular mortality and diabetes.

Background: To assess the value of peptidoglycan recognition protein 2 (PGLYRP2) in assessing the disease activity and lipid metabolism in patients with systemic lupus erythematosus (SLE).

Methods: SLE patients with stable disease (n = 15), active lupus nephritis (LN) (n = 15) and neuropsychiatric systemic lupus erythematosus (NP-SLE) (n = 15) admitted to Northern Jiangsu People's Hospital (Jiangsu, China) in 2019-2020 were recruited. In addition, volunteers with matched age and sex (n = 15) were enrolled as controls. The level of PGLYRP2 in the serum and its expression in peripheral blood mononuclear cells (PBMCs) were measured. The link between PGLYRP2 level and clinical parameters (including lipid profile) was described.

Results: Serum PGLYRP2 level in SLE cases exceeded that in healthy volunteers (3938.56 ± 576.07 pg/mL), and significantly higher in active LN (5152.93 ± 446.13 pg/mL) and NP-SLE patients (5141.52 ± 579.61 pg/mL). As shown by quantitative real-time PCR results, the expression of PGLYRP2 in PBMCs of SLE patients with active LN and NP-SLE surpassed that in healthy volunteers (P < 0.01). Receiver operating characteristic (ROC) curves demonstrated that PGLYRP2 was capable of distinguishing stable SLE from active LN (AUC = 0.841, 95%CI = 0.722-0.960, P = 0.000). PGLYRP2 level positively correlated with SLEDAI of SLE patients (r = 0.5783, P < 0.01). Moreover, its level varied with serological and renal function parameters (complement 3, complement 4, estimated glomerular filtration rate and 24-h urine protein) and immunoglobulin A (IgA) of SLE. A potential correlation between PGLYRP2 level and lipid profile (HLD-c, Apo-A1 and Apo B/A1) was determined in SLE patients. The linear regression analysis indicated SLEDAI as an independent factor of PGLYRP2 level, with a positive correlation in between (P < 0.05).

Conclusions: Serum PGLYRP2 level significantly increases in SLE patients, and is positively correlated to SLEDAI. Moreover, serum PGLYRP2 level is correlated with renal damage parameters and the abnormal lipid profile of SLE. PGLYRP2 could be used to predict SLE activity, dyslipidemia and cardiovascular disease risks in SLE patients.

Keywords: Lipid profile; PGLYRP2; SLE disease activity index; Systemic lupus erythematosus.

The aim of this study was to investigate lipid profiles in patients with end-stage renal disease receiving hemodialysis (HD), continuous ambulatory peritoneal dialysis (CAPD), or no dialysis (nondialytic treatment group, NT), and to analyze the association between dyslipidemia in CAPD patients with glucose-containing dialysate dosages. Lipid profiles were determined in 64 NT patients, 62 HD patients, and 180 CAPD patients at a single time point. NT patients' samples were collected following hospitalization due to renal failure. HD and CAPD patients' samples were collected after 3 months of dialysis. The association between lipid profiles of 180 CAPD patients and glucose-containing dialysate was analyzed using Pearson methods; 76.56% of NT patients, 66.13% of HD patients, and 72.22% of CAPD patients had dyslipidemia. Compared with NT patients, CAPD patients had significantly altered levels of cholesterol, triglycerides, high-density lipoprotein, apolipoproein (Apo)-A1, and Apo-E (p < 0.05), but unchanged levels of low-density lipoprotein or Apo-B. There was no correlation between the three different concentrations of glucose in the dialysate with the lipid profile of CAPD patients. We concluded that patients on CAPD exhibit dyslipidemia, and that different concentrations of glucose in the dialysate do not affect lipid profiles in these patients.

OBJECTIVE

High-density lipoproteins (HDL) are thought to exert a protective role against atherosclerosis. The measurement of the cholesterol mass within HDL (HDL-C) represents a good biomarker of cardiovascular health, but HDL-C appears to be a poor therapeutic target. Here, we discuss new targets for the development of HDL-directed therapies.

RESULTS

Among cardio-protective functions of HDL particles, the ability of HDL to remove cholesterol from cells involved in the early stages of atherosclerosis is considered one of the most important functions. This process, termed "HDL biogenesis," is initiated by the formation of highly specialized plasma membrane micro-domains by the ATP-binding cassette transporter A1 (ABCA1) and the binding of apolipoproteins (apo) such as apoA-I, the major protein moiety of HDL, to the micro-domains. Although early strategies aimed at increasing HDL biogenesis by upregulating ABCA1 or apoA-I gene expression have not met with clinical success, recent advances in understanding transcriptional, post-transcriptional, and post-translational regulatory pathways propose new targets for the promotion of HDL biogenesis. We have recently reported that a novel apoA-I-binding protein desmocollin 1 (DSC1) prevents HDL biogenesis and that inhibition of apoA-I-DSC1 interactions promotes HDL biogenesis by stabilizing ABCA1. This new HDL regulation pathway nominates DSC1 as an attractive pharmacological target. In the absence of clinically useful therapy to increase HDL biogenesis, finding novel targets to unlock the therapeutic potential of HDL is highly desired. Modulation of apoA-I-DSC1 interactions may be a viable strategy.

Purpose: The study explored the association of waist circumference (WC) with the severity of cardiovascular diseases and hospital readmission of coronary artery disease (CAD) patients with normal body mass index (BMI).

Patients and methods: 213 female and 431 male normal-BMI CAD patients were enrolled and assigned in three groups based on their gender-specific WC tertiles. Their cardiovascular risk factors and coronary angiography characteristics were analyzed in a cross-sectional study, and the gender-specific relationship between WC and one-year re-admission rate was prospectively explored.

Results: The cross-sectional analysis showed that for male normal-BMI CAD patients, diabetes and dyslipidemia prevalence, Apo B/A1, hs-CRP, and uric acid levels triglycerides-glucose index, the incidence of left main disease, three vessel disease, calcification lesion, total occlusive lesion, and complex lesion, as well as Gensini score was in the order of WC tertile 3 > WC tertile 2 > WC tertile 1. In addition, male normal-BMI CAD patients in the highest WC tertile were at an increased risk of severe CAD (OR=2.21), and the correlation was still statistically significant even after adjusting for potential cardiovascular risk factors (OR=1.87). For female normal-BMI CAD patients, as the WC tertiles increased, uric acid level, the prevalence of three vessel disease, diffuse lesion, and complex lesion gradually increased (P <0.05), but no significant difference was found in the risk of severe CAD among different WC groups (all P >0.05). Prospective analyses showed that the higher the WC tertile was, the higher the one-year re-admission rate in men, but not in women, and after adjusting for other risk factors, men with the highest WC tertile showed more than twice the risk of patients with the lowest WC tertile.

Conclusion: Male but not female, normal-BMI CAD patients with increased WC had more severe CAD and a higher risk of one-year re-admission rate.

Keywords: coronary artery disease; normal body mass index; one-year re-admission with adverse cardiovascular event; severe CAD; waist circumference.

Background & aims: To examine the relationship between changes in skeletal muscle mass and lipid metabolism and glycometabolism in patients with rheumatoid arthritis (RA).

Methods: Data were analyzed from 148 female RA patients and 145 age-matched non-RA (control) female subjects from a prospective cohort study (TOMORROW; TOtal Management Of Risk factors in Rheumatoid arthritis patients to lOWer morbidity and mortality study). Appendicular skeletal muscle mass (ASM) was assessed using dual-energy x-ray absorptiometry and skeletal muscle mass index (SMI) was calculated as ASM divided by the square of height. The reference value for SMI in Asian women, 5.4 kg/m², was used to define low SMI. Data were assessed using cross-sectional (2010 baseline data) and longitudinal (change in value from 2010 to 2013) methods from the retrospective cohort.

Results: At baseline in RA patients, the low SMI group showed significantly higher low-density lipoprotein cholesterol (LDL-chol) (p = 0.015), apolipoprotein (Apo)B (p = 0.046), and ApoB-to-A1 (ApoB/A1) (p = 0.025) than the normal SMI group. In multiple regression analysis of RA patients, sequential changes from 2010 to 2013 (Δ) in SMI and ApoB and ApoC2 showed significant negative relationships (β = -0.19, -0.18, respectively) even after adjusting for age, RA duration, exercise habits, medication for RA, disease severity, activities of daily living (ADL) and body fat mass. No significant relation was evident between ΔSMI and various glycometabolism parameters in RA patients.

Conclusions: Skeletal muscle mass might be related to lipid metabolism in RA patients. This relationship is independent of factors such as disease severity and body fat mass.

Keywords: Body composition; Cachexia; Dyslipidemia; Nutrition; Sarcopenia; Skeletal muscle.

Background: Erectile dysfunction (ED) is closely related to coronary heart disease (CHD). Apolipoprotein (Apo) A1, Apo B, and Apo A/Apo B are known to be predictive factors for CHD. They are not yet a definite laboratory marker for the diagnosis of ED in cardiology. Therefore, we investigated the association between Apo A1, Apo B, and Apo A/Apo B, and ED.

Aim: To investigate the association between Apo A, Apo B, and Apo A/Apo B and the severity of ED.

Methods: A total of 152 ED patients and 39 healthy control participants underwent a fasting blood draw to test for Apo A, Apo B, and Apo A/Apo B and a detailed laboratory examination. The International Erectile Function Index (IIEF-5) was used to determine the severity of ED. Receiver operating characteristic (ROC) curve analysis was performed to identify the cutoff values for Apo A, Apo B, and Apo A/Apo B. Each questionnaire was completed before any diagnosis was made or treatment performed.

Outcomes: Several lipid profile indicators (Apo A, Apo B, Apo A/Apo B, lipoprotein (a), free fatty acids, and total cholesterol) were studied, along with several questionnaires.

Results: In our study, the number of patients with no ED, mild ED, mild-to-moderate ED, and moderate-to-severe ED were 39 (20.4%), 58 (30.4%), 36 (18.8%), and 58 (30.4%), respectively. Apo A and Apo A/Apo B were significantly reduced in patients with more severe ED (P = .037 and P < .001, respectively), while Apo B was significantly increased in patients with more severe ED (P = .002). According to the ROC curve, Apo A/Apo B had a medium diagnostic value for risk of ED with an AUC of 0.743 (95% CI: 0.68-0.80). For moderate-to-severe ED, 3 apolipoprotein indexes, including Apo B, Apo A, and Apo A/Apo B had medium diagnostic performance with AUCs of 0.759 (95% CI: 0.66-0.84), 0.703 (95% CI: 0.60-0.79), and 0.808 (95% CI: 0.72-0.88), respectively.

Clinical implications: Our results can inform cardiologists in the assessment of ED in patients with CHD.

Strengths and limitations: This study is the first to investigate the association between apolipoprotein and ED in China. The major limitations are that our sample size was too small to have matched controls without ED for different Apo levels.

Conclusion: Our results showed that Apo B, Apo A, and Apo A/Apo B can be used as markers to evaluate the risk of ED and that these proteins play an important role in the etiology of ED. Li X, Li D. The Suggestive Effect of Apo A, Apo B, and Apo A/Apo B on Erectile Dysfunction. J Sex Med 2020;XX:XXX-XXX.

Keywords: Apo A/Apo B; Apolipoprotein A; Apolipoprotein B; Coronary Heart Disease Risk Factors; Diagnosis; Erectile Dysfunction.

A study of conditions for the elution of apo A1 and B lipoproteins from dried blood spots has led to the development of an apo B/A1 ratio assay with results for dried blood spots which are comparable with serum assays. This assay has been developed to be suitable for large scale population screening. The concept of measuring ratios for co-eluting blood constituents improves the accuracy and precision of blood spot assays and opens up the possibility that patients could take their own blood sample and send it to the laboratory by post.

Objectives: Cardiovascular diseases (CVDs) are responsible of 31% of all deaths worldwide. Genetic predisposition to CVDs in adolescents remains largely unknown. Aims of present research are to examine the association of ADIPOQ gene polymorphisms with cardiovascular disease risk factors in European adolescents.

Methods: A total of 14 polymorphisms in the ADIPOQ gene were genotyped in 1057 European adolescents (12-18 years old) from the Healthy Lifestyle in Europe by Nutrition in Adolescence Cross-Sectional Study. We measured serum lipids and a CVD risk score, along with weight, height, triceps, and subscapular skinfold thickness, leptin, insulin and other markers of glucose regulation.

Results: The rs822393, rs822395 and rs7649121 polymorphisms of ADIPOQ gene were significantly associated with several CVD risk factors [i.e. high-density lipoprotein cholesterol (HDL-C), apolipoprotein (Apo) A1, SBP and CVD risk score] in European adolescents. We also found an association of the TGAAGT ADIPOQ haplotype (rs822393, rs16861210, rs822395, rs822396, rs12495941 and rs7649121) with HDL-C and ApoA1 levels.

Conclusion: Several individual polymorphisms (rs822393, rs822395 and rs7649121) and a haplotype of ADIPOQ gene were significantly associated with cardiovascular disease risk factors in European adolescents.

The main apolipoproteins in HDL are known to be apo A1, A2, and A4. Apolipoprotein (mainly apo A1) were isolated and purified from about 100 liters of rabbit's serum for the purpose of studying their inhibitory effect on the development of atheromatous plaques in rabbits. Data indicated that lipid content in aortic intima: lipid deposition in intima morphologically; area of atheromatous lesion involved and the severity of atheromatous lesions obtained were much lower in animals of the experimental group after intravenous administration of apolipoproteins isolated from HDL for 8 to 12 weeks than those in animals of the cholesterol control groups in two successive experiments. In accordance with data obtained from epidemiological and experimental surveys. HDL level was known to be correlated reversely with the incidence of atherosclerosis. Data of these experiments confirmed that apolipoproteins (mainly apoA1) in HDL are the main factors of this inhibitory effect. This result provides a scientific basis for the measurement of preparation of certain apolipoproteins (apo A1 and possibly A1) by high bio-technology for prevention and treatment of atherosclerosis in the near future.

Atherosclerosis is the primary disease in the majority of patients with ischemic brain disease (IBD). Etiopathogenesis of atherosclerosis has not been more precisely defined, but risk factors significant for its generation and development, so as for IBD development, have been identified. They were designated as risk factors for brain atherosclerosis (RFBA). The aim of this study was to establish the frequency and significance of RFBA association in the patients with acute IBD in relation to IBD severity. The investigation included 60 patients with AIBD. RFBA were: arterial hypertension, dyslipoproteinemia, diabetes and smoking. For all the patients included in the study detailed history was noted, daily glycemia profile was done, blood pressure was measured 3 times a day and parameters of lipid status with counting of LDL/HDL indices and Apo A1/Apo B were determined. IBD was confirmed by computerized tomography of brain. The degree of IBD severity was determined in all the patients by Grotta's scale. After the statistical processing, the results of the research showed that in the patients with IBD the most frequent were arterial hypertension, then smoking, dyslipoproteinemia and diabetes. In significant number of patients existed association of several factors, which was in significant positive correlation with the degree of IBD severity. It was concluded that risk factors for atherosclerosis were simultaneously risk factors for IBD. IBD is the most severe, final stage in evolution of brain atherosclerosis.

The important role of remnant lipoprotein, which is linked up to serum insulin, in the development of atherosclerosis is well known. So, measurement of remnant has a benefit as the indicator of cardiovascular disease-risk. Recently, Nakajima et al have developed a simple, rapid assay method, using a immunoaffinity gel mixture of anti-apo B-100 and anti-apo A1 monoclonal antibodies coupled with Sepharose 4B. The apoprotein composition of RLP which is unbound with mixed gel is as similar to apo-E rich VLDL. Clinical significance of RLP-C has been already indicated by many reports.