Apolipoprotein C-I: A 6.6-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS; INTERMEDIATE-DENSITY LIPOPROTEINS; and HIGH-DENSITY LIPOPROTEINS. Apo C-I displaces APO E from lipoproteins, modulate their binding to receptors (RECEPTORS, LDL), and thereby decrease their clearance from plasma. Elevated Apo C-I levels are associated with HYPERLIPOPROTEINEMIA and ATHEROSCLEROSIS.Apolipoproteins C: A group of apolipoproteins that can readily exchange among the various classes of lipoproteins (HDL; VLDL; CHYLOMICRONS). After lipolysis of TRIGLYCERIDES on VLDL and chylomicrons, Apo-C proteins are normally transferred to HDL. The subtypes can modulate remnant binding to receptors, LECITHIN CHOLESTEROL ACYLTRANSFERASE, or LIPOPROTEIN LIPASE.Apolipoprotein C-III: A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS and CHYLOMICRON REMNANTS. Apo C-III, synthesized in the liver, is an inhibitor of LIPOPROTEIN LIPASE. Apo C-III modulates the binding of chylomicron remnants and VLDL to receptors (RECEPTORS, LDL) thus decreases the uptake of triglyceride-rich particles by the liver cells and subsequent degradation. The normal Apo C-III is glycosylated. There are several polymorphic forms with varying amounts of SIALIC ACID (Apo C-III-0, Apo C-III-1, and Apo C-III-2).Lipoproteins, VLDL: A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues.TriglyceridesApolipoprotein A-I: The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.Apolipoproteins E: A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.Apolipoprotein B-100: A 513-kDa protein synthesized in the LIVER. It serves as the major structural protein of low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). It is the ligand for the LDL receptor (RECEPTORS, LDL) that promotes cellular binding and internalization of LDL particles.Apolipoproteins B: Major structural proteins of triacylglycerol-rich LIPOPROTEINS. There are two forms, apolipoprotein B-100 and apolipoprotein B-48, both derived from a single gene. ApoB-100 expressed in the liver is found in low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). ApoB-48 expressed in the intestine is found in CHYLOMICRONS. They are important in the biosynthesis, transport, and metabolism of triacylglycerol-rich lipoproteins. Plasma Apo-B levels are high in atherosclerotic patients but non-detectable in ABETALIPOPROTEINEMIA.Apolipoprotein E4: A major and the second most common isoform of apolipoprotein E. In humans, Apo E4 differs from APOLIPOPROTEIN E3 at only one residue 112 (cysteine is replaced by arginine), and exhibits a lower resistance to denaturation and greater propensity to form folded intermediates. Apo E4 is a risk factor for ALZHEIMER DISEASE and CARDIOVASCULAR DISEASES.Apolipoprotein E3: A 34-kDa glycosylated protein. A major and most common isoform of apolipoprotein E. Therefore, it is also known as apolipoprotein E (ApoE). In human, Apo E3 is a 299-amino acid protein with a cysteine at the 112 and an arginine at the 158 position. It is involved with the transport of TRIGLYCERIDES; PHOSPHOLIPIDS; CHOLESTEROL; and CHOLESTERYL ESTERS in and out of the cells.Apolipoprotein A-II: The second most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. It has a high lipid affinity and is known to displace APOLIPOPROTEIN A-I from HDL particles and generates a stable HDL complex. ApoA-II can modulate the activation of LECITHIN CHOLESTEROL ACYLTRANSFERASE in the presence of APOLIPOPROTEIN A-I, thus affecting HDL metabolism.Apolipoproteins: Protein components on the surface of LIPOPROTEINS. They form a layer surrounding the hydrophobic lipid core. There are several classes of apolipoproteins with each playing a different role in lipid transport and LIPID METABOLISM. These proteins are synthesized mainly in the LIVER and the INTESTINES.Apolipoprotein C-II: A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS. It contains a cofactor for LIPOPROTEIN LIPASE and activates several triacylglycerol lipases. The association of Apo C-II with plasma CHYLOMICRONS; VLDL, and HIGH-DENSITY LIPOPROTEINS is reversible and changes rapidly as a function of triglyceride metabolism. Clinically, Apo C-II deficiency is similar to lipoprotein lipase deficiency (HYPERLIPOPROTEINEMIA TYPE I) and is therefore called hyperlipoproteinemia type IB.Apolipoproteins A: Structural proteins of the alpha-lipoproteins (HIGH DENSITY LIPOPROTEINS), including APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II. They can modulate the activity of LECITHIN CHOLESTEROL ACYLTRANSFERASE. These apolipoproteins are low in atherosclerotic patients. They are either absent or present in extremely low plasma concentration in TANGIER DISEASE.Apolipoprotein E2: One of three major isoforms of apolipoprotein E. In humans, Apo E2 differs from APOLIPOPROTEIN E3 at one residue 158 where arginine is replaced by cysteine (R158--C). In contrast to Apo E3, Apo E2 displays extremely low binding affinity for LDL receptors (RECEPTORS, LDL) which mediate the internalization and catabolism of lipoprotein particles in liver cells. ApoE2 allelic homozygosity is associated with HYPERLIPOPROTEINEMIA TYPE III.Apolipoprotein B-48: A 241-kDa protein synthesized only in the INTESTINES. It serves as a structural protein of CHYLOMICRONS. Its exclusive association with chylomicron particles provides an indicator of intestinally derived lipoproteins in circulation. Apo B-48 is a shortened form of apo B-100 and lacks the LDL-receptor region.Lipoproteins, HDL: A class of lipoproteins of small size (4-13 nm) and dense (greater than 1.063 g/ml) particles. HDL lipoproteins, synthesized in the liver without a lipid core, accumulate cholesterol esters from peripheral tissues and transport them to the liver for re-utilization or elimination from the body (the reverse cholesterol transport). Their major protein component is APOLIPOPROTEIN A-I. HDL also shuttle APOLIPOPROTEINS C and APOLIPOPROTEINS E to and from triglyceride-rich lipoproteins during their catabolism. HDL plasma level has been inversely correlated with the risk of cardiovascular diseases.Apoprotein(a): A large and highly glycosylated protein constituent of LIPOPROTEIN (A). It has very little affinity for lipids but forms disulfide-linkage to APOLIPOPROTEIN B-100. Apoprotein(a) has SERINE PROTEINASE activity and can be of varying sizes from 400- to 800-kDa. It is homologous to PLASMINOGEN and is known to modulate THROMBOSIS and FIBRINOLYSIS.Lipoproteins: Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.Lipoprotein(a): A lipoprotein that resembles the LOW-DENSITY LIPOPROTEINS but with an extra protein moiety, APOPROTEIN (A) also known as APOLIPOPROTEIN (A), linked to APOLIPOPROTEIN B-100 on the LDL by one or two disulfide bonds. High plasma level of lipoprotein (a) is associated with increased risk of atherosclerotic cardiovascular disease.Apolipoproteins D: A glycoprotein component of HIGH-DENSITY LIPOPROTEINS that transports small hydrophobic ligands including CHOLESTEROL and STEROLS. It occurs in the macromolecular complex with LECITHIN CHOLESTEROL ACYLTRANSFERASE. Apo D is expressed in and secreted from a variety of tissues such as liver, placenta, brain tissue and others.Lipoproteins, LDL: A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.Lipids: A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)Receptors, LDL: Receptors on the plasma membrane of nonhepatic cells that specifically bind LDL. The receptors are localized in specialized regions called coated pits. Hypercholesteremia is caused by an allelic genetic defect of three types: 1, receptors do not bind to LDL; 2, there is reduced binding of LDL; and 3, there is normal binding but no internalization of LDL. In consequence, entry of cholesterol esters into the cell is impaired and the intracellular feedback by cholesterol on 3-hydroxy-3-methylglutaryl CoA reductase is lacking.Atherosclerosis: A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.Cholesterol, HDL: Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.Arteriosclerosis: Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Hyperlipoproteinemia Type III: An autosomal recessively inherited disorder characterized by the accumulation of intermediate-density lipoprotein (IDL or broad-beta-lipoprotein). IDL has a CHOLESTEROL to TRIGLYCERIDES ratio greater than that of VERY-LOW-DENSITY LIPOPROTEINS. This disorder is due to mutation of APOLIPOPROTEINS E, a receptor-binding component of VLDL and CHYLOMICRONS, resulting in their reduced clearance and high plasma levels of both cholesterol and triglycerides.Phosphatidylcholine-Sterol O-Acyltransferase: An enzyme secreted from the liver into the plasma of many mammalian species. It catalyzes the esterification of the hydroxyl group of lipoprotein cholesterol by the transfer of a fatty acid from the C-2 position of lecithin. In familial lecithin:cholesterol acyltransferase deficiency disease, the absence of the enzyme results in an excess of unesterified cholesterol in plasma. EC 2.3.1.43.Cholesterol, LDL: Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.Zinc Fingers: Motifs in DNA- and RNA-binding proteins whose amino acids are folded into a single structural unit around a zinc atom. In the classic zinc finger, one zinc atom is bound to two cysteines and two histidines. In between the cysteines and histidines are 12 residues which form a DNA binding fingertip. By variations in the composition of the sequences in the fingertip and the number and spacing of tandem repeats of the motif, zinc fingers can form a large number of different sequence specific binding sites.Deoxyribonucleases: Enzymes which catalyze the hydrolases of ester bonds within DNA. EC 3.1.-.Endonucleases: Enzymes that catalyze the hydrolysis of the internal bonds and thereby the formation of polynucleotides or oligonucleotides from ribo- or deoxyribonucleotide chains. EC 3.1.-.Gene Targeting: The integration of exogenous DNA into the genome of an organism at sites where its expression can be suitably controlled. This integration occurs as a result of homologous recombination.Targeted Gene Repair: A technique which uses synthetic oligonucleotides to direct the cell's inherent DNA repair system to correct a mutation at a specific site in an episome or chromosome.FluorobenzenesParturient Paresis: A disease of pregnant and lactating cows and ewes leading to generalized paresis and death. The disease, which is characterized by hypocalcemia, occurs at or shortly after parturition in cows and within weeks before or after parturition in ewes.Hydroxymethylglutaryl CoA Reductases: Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.Hypertriglyceridemia: A condition of elevated levels of TRIGLYCERIDES in the blood.Cacao: A tree of the family Sterculiaceae (or Byttneriaceae), usually Theobroma cacao, or its seeds, which after fermentation and roasting, yield cocoa and chocolate.Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.Promoter Regions, Genetic: DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.Transcription, Genetic: The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.Electrophoretic Mobility Shift Assay: An electrophoretic technique for assaying the binding of one compound to another. Typically one compound is labeled to follow its mobility during electrophoresis. If the labeled compound is bound by the other compound, then the mobility of the labeled compound through the electrophoretic medium will be retarded.Catechin: An antioxidant flavonoid, occurring especially in woody plants as both (+)-catechin and (-)-epicatechin (cis) forms.Docosahexaenoic Acids: C22-unsaturated fatty acids found predominantly in FISH OILS.Polymorphism, Genetic: The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.Fatty Acids, Omega-3: A group of fatty acids, often of marine origin, which have the first unsaturated bond in the third position from the omega carbon. These fatty acids are believed to reduce serum triglycerides, prevent insulin resistance, improve lipid profile, prolong bleeding times, reduce platelet counts, and decrease platelet adhesiveness.Fatty Acids: Organic, monobasic acids derived from hydrocarbons by the equivalent of oxidation of a methyl group to an alcohol, aldehyde, and then acid. Fatty acids are saturated and unsaturated (FATTY ACIDS, UNSATURATED). (Grant & Hackh's Chemical Dictionary, 5th ed)Alleles: Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.

Allele-specific differences in apolipoprotein C-III mRNA expression in human liver. (1/417)

BACKGROUND: Sequence variations at the apolipoprotein (apo)C-III gene locus have been associated with increased plasma triglycerides. In particular, the S2 allele of an SstI polymorphism in the 3' untranslated region has been associated with hypertriglyceridemia in many populations. The aim of this study was to determine whether the variant S2 allele is related to increased mRNA expression in vivo. METHODS: We measured allele-specific apoC-III expression in liver biopsies of five obese subjects, using restriction isotyping and a primer extension method, both based on the SstI polymorphism. RESULTS: The expression of mRNA by the S1 and S2 alleles was similar in two patients, whereas the mRNA encoded by the S2 allele was 14%, 26%, and 29% more abundant than the wild-type mRNA in the remaining three patients. Because other polymorphisms at the apoC-III gene locus have been implicated in the S2-associated hypertriglyceridemia, we determined apoC-III haplotypes comprising promoter polymorphisms at -935, -641, -630, -625, -482, -455, as well as the SstI sites and a BbvI site, both located in the 3' untranslated region. None of these polymorphisms nor any haplotype exhibited a perfect association with allele-specific expression, but variation at the T-482C site correlated in four of five subjects with the relative allele abundance. CONCLUSION: These data provide preliminary evidence for allele-specific differences in apoC-III mRNA expression in vivo and suggest that such differences may contribute to associations of apoC-III gene polymorphisms with hypertriglyceridemia.  (+info)

Vitamin A is linked to the expression of the AI-CIII-AIV gene cluster in familial combined hyperlipidemia. (2/417)

There is growing evidence of the capacity of vitamin A to regulate the expression of the genetic region that encodes apolipoproteins (apo) A-I, C-III, and A-IV. This region in turn has been proposed to modulate the expression of hyperlipidemia in the commonest genetic form of dyslipidemia, familial combined hyperlipidemia (FCHL). The hypothesis tested here was whether vitamin A (retinol), by controlling the expression of the AI-CIII-AIV gene cluster, plays a role in modulating the hyperlipidemic phenotype in FCHL. We approached the subject by studying three genetic variants of this region: a C1100-T transition in exon 3 of the apoC-III gene, a G3206-T transversion in exon 4 of the apoC-III gene, and a G-75-A substitution in the promoter region of the apoA-I gene. The association between plasma vitamin A concentrations and differences in the plasma concentrations of apolipoproteins A-I and C-III based on the different genotypes was assessed in 48 FCHL patients and 74 of their normolipidemic relatives. The results indicated that the subjects carrying genetic variants associated with increased concentrations of apoA-I and C-III (C1100-T and G-75-A) also presented increased plasma concentrations of vitamin A. This was only observed among the FCHL patients, which suggested that certain characteristics of these patients contributed to this association. The G3206-T was not associated with changes in either apolipoprotein concentrations or in vitamin A. In summary, we report a relationship between genetically determined elevations of proteins of the AI-CIII-AIV gene cluster and vitamin A in FCHL patients. More studies will be needed to confirm that vitamin A plays a role in FCHL which might also be important for its potential application to therapeutical approaches.  (+info)

Mass spectral study of polymorphism of the apolipoproteins of very low density lipoprotein. (3/417)

New isoforms of apolipoprotein (apo)C-I and apoC-III have been detected in delipidated fractions from very low density lipoprotein (VLDL) using matrix-assisted laser desorption (MALDI) and electrospray ionization (ESI) mass spectrometry (MS). The cleavage sites of truncated apoC-III isoforms have also been identified. The VLDL fractions were isolated by fixed-angle single-spin ultracentrifugation using a self-generating sucrose density gradient and delipidated using a newly developed C18 solid phase extraction protocol. Fifteen apoC isoforms and apoE were identified in the MALDI spectra and the existence of the more abundant species was verified by ESI-MS. The relative intensities of the apoCs are closely correlated in three normolipidemic subjects. A fourth subject with type V hyperlipidemia exhibited an elevated apoC-III level and a suppressed level of the newly discovered truncated apoC-I isoform. ApoC-II was found to be particularly sensitive to in vitro oxidation. The dynamic range and specificity of the MALDI assay shows that the complete apoC isoform profile and apoE phenotype can be obtained in a single measurement from the delipidated VLDL fraction.  (+info)

Kinetics and mechanism of exchange of apolipoprotein C-III molecules from very low density lipoprotein particles. (4/417)

Transfer of apolipoprotein (apo) molecules between lipoprotein particles is an important factor in modulating the metabolism of the particles. Although the phenomenon is well established, the kinetics and molecular mechanism of passive apo exchange/transfer have not been defined in detail. In this study, the kinetic parameters governing the movement of radiolabeled apoC molecules from human very low density lipoprotein (VLDL) to high density lipoprotein (HDL3) particles were measured using a manganese phosphate precipitation assay to rapidly separate the two types of lipoprotein particles. In the case of VLDL labeled with human [14C]apoCIII1, a large fraction of the apoCIII1 transfers to HDL3 within 1 minute of mixing the two lipoproteins at either 4 degrees or 37 degrees C. As the diameter of the VLDL donor particles is decreased from 42-59 to 23-25 nm, the size of this rapidly transferring apoCIII1 pool increases from about 50% to 85%. There is also a pool of apoCIII1 existing on the donor VLDL particles that transfers more slowly. This slow transfer follows a monoexponential rate equation; for 35-40 nm donor VLDL particles the pool size is approximately 20% and the t1/2 is approximately 3 h. The flux of apoCIII molecules between VLDL and HDL3 is bidirectional and all of the apoCIII seems to be available for exchange so that equilibrium is attained. It is likely that the two kinetic pools of apoCIII are related to conformational variations of individual apo molecules on the surface of VLDL particles. The rate of slow transfer of apoCIII1 from donor VLDL (35-40 nm) to acceptor HDL3 is unaffected by an increase in the acceptor to donor ratio, indicating that the transfer is not dependent on collisions between donor and acceptor particles. Consistent with this, apoCIII1 molecules can transfer from donor VLDL to acceptor HDL3 particles across a 50 kDa molecular mass cutoff semipermeable membrane separating the lipoprotein particles. These results indicate that apoC molecules transfer between VLDL and HDL3 particles by an aqueous diffusion mechanism.  (+info)

CREB-binding protein is a transcriptional coactivator for hepatocyte nuclear factor-4 and enhances apolipoprotein gene expression. (5/417)

Hepatocyte nuclear factor-4 (HNF-4) is a liver-enriched transcription factor that is crucial in the regulation of a large number of genes involved in glucose, cholesterol, and fatty acid metabolism and in determining the hepatic phenotype. We have previously shown that HNF-4 contains transcription activation functions at the N terminus (AF-1) and the C terminus (AF-2) which work synergistically to confer full HNF-4 activity. Here, we show that HNF-4 recruits the CREB-binding protein (CBP) coactivator on promoters of genes that contain functional HNF-4 sites. HNF-4 interacts with the N-terminal region of CBP (amino acids 1-771) and the C-terminal region of CBP (amino acids 1812-2441). The two activating functions of HNF-4, AF-1 and AF-2, interact with the N terminus and the N and C terminus of CBP, respectively. In addition, we show that in contrast to the other nuclear hormone receptors the interaction between HNF-4 and CBP is ligand-independent. Recruitment of CBP by HNF-4 results in an enhancement of the transcriptional activity of the latter. CBP does not activate gene expression in the absence of HNF-4, and dominant negative forms of HNF-4 prevent transcriptional activation by CBP, suggesting that the mere recruitment of CBP by HNF-4 is not sufficient for enhancement of gene expression. These findings demonstrate that CBP acts as a transcriptional coactivator for HNF-4 and provide new insights into the regulatory function of HNF-4.  (+info)

Characterization of remnant-like particles isolated by immunoaffinity gel from the plasma of type III and type IV hyperlipoproteinemic patients. (6/417)

Previous studies have investigated the potential atherogenicity and thrombogenicity of triglyceride-rich lipoprotein (TRL) remnants by isolating them from plasma within a remnant-like particle (RLP) fraction, using an immunoaffinity gel containing specific anti-apoB-100 and anti-apoA-I antibodies. In order to characterize lipoproteins in this RLP fraction and to determine to what extent their composition varies from one individual to another, we have used automated gel filtration chromatography to determine the size heterogeneity of RLP isolated from normolipidemic control subjects (n = 8), and from type III (n = 6) and type IV (n = 9) hyperlipoproteinemic patients, who by selection had similarly elevated levels of plasma triglyceride (406 +/- 43 and 397 +/- 35 mg/dl, respectively). Plasma RLP triglyceride, cholesterol, apoB, apoC-III, and apoE concentrations were elevated 2- to 6-fold (P < 0. 05) in hyperlipoproteinemic patients compared to controls. RLP fractions of type III patients were enriched in cholesterol and apoE compared to those of type IV patients, and RLP of type IV patients were enriched in triglyceride and apoC-III relative to those of normolipidemic subjects. In normolipidemic subjects, the majority of RLP had a size similar to LDL or HDL. The RLP of hyperlipoproteinemic patients were, however, larger and were similar in size to TRL, or were intermediate in size (i.e., ISL) between that of TRL and LDL. Compared to controls, ISL in the RLP fraction of type III patients were enriched in apoE relative to apoC-III, whereas in type IV patients they were enriched in apoC-III relative to apoE. These results demonstrate that: 1) RLP are heterogeneous in size and composition in both normolipidemic and hypertriglyceridemic subjects, and 2) the apoE and apoC-III composition of RLP is different in type III compared to type IV hyperlipoproteinemic patients.  (+info)

ApoCIII gene variants modulate postprandial response to both glucose and fat tolerance tests. (7/417)

BACKGROUND: We investigated the relationship between variation in the apolipoprotein (apo) AI-CIII-AIV gene cluster and response to an oral glucose test (OGTT) and oral fat load test (OFTT) in the EARSII group of young, healthy male offspring whose fathers had had a myocardial infarction before the age of 55 years (cases, n=407) compared with age-matched controls (n=415). The apoCIII variations examined were C3238G (SstI) in the 3'-UTR, C1100T in exon 3, C-482T in the insulin response element (IRE), and T-2854G in the apoCIII-AIV intergenic region. METHODS AND RESULTS: The postprandial response was regulated by variation at the T-2854G and C3238G sites. After the OFTT, carriers of the rare alleles had delayed clearance of triglyceride (Tg) levels; G-2854 carriers showed the largest effect on Tg (AUC, 24% greater, P<0.002; peak, 19% greater, P<0.005), and G3238 carriers showed a smaller response (AUC, 13% greater, P<0.05; peak, 13% greater, P=0.03). However, after adjustment for fasting level of Tg, only the effect with the T-2854G remained significant. Variation at the C-482T (IRE) determined response to the OGTT, with carriers of the rare T-482 having significantly elevated glucose (28.7% AUC, P=0.013) and insulin (20.5% AUC, P<0. 01) concentrations. CONCLUSIONS: These data suggest that specific genetic variants at the apoCIII gene locus differentially affect postprandial and response to OGTT and suggest a novel mechanism for the effects of variation at this locus on risk for atherosclerosis.  (+info)

Apolipoprotein B-containing lipoproteins in renal failure: the relation to mode of dialysis. (8/417)

BACKGROUND: The aim of this study was to establish whether there is a differential effect of mode of dialysis, hemodialysis (HD), or continuous ambulatory peritoneal dialysis (CAPD) on the dyslipidemia of renal failure. METHODS: The lipoprotein profile was determined in 61 non-diabetic patients on chronic HD (N = 30) and CAPD treatment (N = 31), and in a control group of 27 healthy subjects. The analysis included the measurement of individual apolipoprotein (apo) A- and apo B-containing lipoproteins (LPs) separated by sequential immunoaffinity chromatography. Apo A-containing lipoproteins include lipoprotein A-I with apo A-I and lipoprotein A-I:A-II with apo A-I and apo A-II as the main protein constituents, whereas apo B-containing lipoproteins comprise simple cholesterol-rich lipoprotein B (LP-B), with apo B as the only protein moiety and complex triglyceride (TG)-rich lipoprotein B complex (LP-Bc) particles with apo B, apo A-II, apo C, and/or apo E as the protein constituents. RESULTS: CAPD patients had significantly higher concentrations of total cholesterol (6.8 vs. 5.1 mmol/liter), low-density lipoprotein (LDL) cholesterol (4.6 vs. 3.2 mmol/liter), TG (2.3 vs. 1.5 mmol/liter), apo B (155.3 vs. 105.7 mg/dl), LP-B (136.0 vs. 91.9 mg/dl), and LP-Bc (19.3 vs. 13.8 mg/dl) than HD patients. Both HD and CAPD patients had significantly higher TG, VLDL cholesterol, apo C-III, and apo E and significantly lower high-density lipoprotein cholesterol, apo A-II, and lipoprotein A-I:A-II levels than control subjects. The distribution of apo C-III in high-density lipoprotein and VLDL-LDL was altered in CAPD patients in comparison with control subjects. This suggests that the removal of TG-rich lipoproteins is less efficient in patients on CAPD. Normotriglyceridemic (NTG; TG < or = 1.7 mmol/liter, 150 mg/dl) CAPD patients had significantly higher levels of TC, LDL cholesterol, apo B, and LP-B than NTG-HD patients. There was little difference in the LP-Bc levels between NTG-CAPD, NTG-HD, and controls. Similarly, hypertriglyceridemic (HTG) CAPD patients had significantly higher TC, LDL cholesterol, apo B, and LP-B levels than HTG-HD patients. The LP-Bc levels were significantly increased in HTG-HD and HTG-CAPD patients compared with controls, but the slightly higher levels in the CAPD patients did not differ significantly from the HD group. CONCLUSION: CAPD and HD patients have a lipoprotein profile characteristic of renal failure. Patients on long-term CAPD have higher levels of cholesterol-rich apo B-containing lipoproteins unrelated to TG levels. Many patients on CAPD also have a substantial elevation of the plasma concentrations of TG-rich LPs. The clinical significance of increased levels of potentially atherogenic LP-B during CAPD remains to be investigated.  (+info)

Background: Apolipoprotein C-III (apoC-III) inhibits lipoprotein lipase activity and hepatic uptake of triglyceride-rich lipoproteins. Elevated levels of apoC-III have been found to be an independent predictor for CHD risk and genetically reduced apoC-III is associated with protection from CHD, making apoC-III a therapeutic target. Omega-3 fatty acid formulations containing docosahexaenoic acid (DHA) have been shown to increase LDL-C in patients with severe hypertriglyceridemia (HTG). Clinical data suggest that eicosapentaenoic acid (EPA) alone, which lowers triglycerides to a similar extent as EPA + DHA, does not raise LDL-C, but also fails to lower apoC-III. Materials: The EVOLVE trial evaluated 2, 3, and 4 g/d of a novel omega-3 free-fatty acid (FFA) formulation containing both EPA + DHA compared with 4 g/d of olive oil. In 399 patients with severe HTG we evaluated the effects on plasma apoC-III levels and the correlations between change in apoC-III and change in plasma lipids (TG, LDL-C) ...
We provide new information on the dose-ranging effect of rosuvastatin, a potent HMG-CoA (or 3-hydroxy-3-methyl-glutaryl-CoA) reductase inhibitor, on VLDL apoC-III metabolism in subjects with the metabolic syndrome. We demonstrated that rosuvastatin dose-dependently decreased VLDL apoC-III concentrations by increasing the FCR and decreasing the PR of VLDL apoC-III. These results add further to our work on the dose-dependent effect of rosuvastatin on apoB-containing lipoproteins and HDL particle kinetics in the same subjects (13,14).. Hypertriglyceridemia in insulin-resistant states, including the metabolic syndrome, results from overproduction and reduced catabolism of TRL and their remnants. These kinetic aberrations may be related to altered VLDL apoC-III metabolism. Previous studies demonstrated that overproduction of VLDL apoC-III explained the higher VLDL apoC-III concentration in these subjects (17). The increased VLDL apoC-III concentration and production rate were associated with elevated ...
Apolipoprotein CIII (apoCIII) is an independent risk for coronary heart disease (CHD). In this study, we investigated the associations among plasma apoCIII, hs-CRP and TNF-α levels and their roles in the clinical features of CHD in the Li and Han ethnic groups in China. A cohort of 474 participants was recruited (238 atherosclerotic patients and 236 healthy controls) from the Li and Han ethnic groups. Blood samples were obtained to evaluate apoCIII, TNF-α, hs-CRP and lipid profiles. Chi-squared, t-tests, and Kruskal-Wallis or Wilcoxon-Mann-Whitney tests, Pearson or Spearman correlation tests and multiple unconditional logistic regression were employed to analyze lipid profiles and variations in plasma apoCIII, TNF-α, hs-CRP in subgroups of CHD and their contributions to CHD using SPSS version 20.0 software. Compared to healthy participants, unfavorable lipid profiles were identified in CHD patients with enhanced systolic pressure, diastolic pressure, fasting blood sugar (FBS), TG, TC, LDL-C, apoB, Lp
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RAPOSO, HELENA F.... Apolipoprotein CIII overexpression exacerbates diet-induced obesity due to adipose tissue higher exogenous lipid uptake and retention and lower lipolysis rates. NUTRITION & METABOLISM 12 n. p. DEC 23 2015. Journal article.
C H Bolton, A P Corfield, L G Downs; Sialidase Activity Acting on Apolipoprotein CIII 1 and 2 in Human Leukocytes and Platelets. Clin Sci (Lond) 1 January 1984; 67 (s9): 15P. doi: https://doi.org/10.1042/cs067015P. Download citation file:. ...
Recent development in gene targeting tools makes production of knockout (KO) rabbits possible. In the present work, we generated five...
C2C12 myotubes exposed to VLDL showed increased levels of ER stress and inflammatory markers whereas peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) and AMP-activated protein kinase (AMPK) levels were reduced and the insulin signalling pathway was attenuated. The effects of VLDL were also observed in isolated skeletal muscle incubated with VLDL. The changes caused by VLDL were dependent on extracellular signal-regulated kinase (ERK) 1/2 since they were prevented by the ERK1/2 inhibitor U0126 or by knockdown of this kinase by siRNA transfection. ApoCIII mimicked the effects of VLDL and its effects were also blocked by ERK1/2 inhibition, suggesting that this apolipoprotein was responsible for the effects of VLDL. Skeletal muscle from transgenic mice overexpressing apoCIII showed increased levels of some ER stress and inflammatory markers and increased phosphorylated ERK1/2 levels, whereas PGC-1α levels were reduced, confirming apoCIII effects in vivo. Finally, incubation ...
Results A higher triglyceride/cholesterol ratio of LDL was found more in HCV-infected donors than in healthy volunteers, and the triglyceride/cholesterol ratio of LDL-LVP was much increased, suggesting that the LPL hydrolysis of triglyceride may be impaired. VLDL, VLDL-LVP, LDL-LVP, but not LDL, suppressed LPL lipolytic activity, which was restored by antibodies that recognised apoC-III/-IV and correlated with the steadily abundant apoC-III/-IV quantities in those particles. In a cell-based system, treatment with VLDL and LVPs reversed the LPL-mediated inhibition of HCV infection in apoC-III/-IV-dependent manners. A multivariate logistic regression revealed that plasma HCV viral loads correlated negatively with LPL lipolytic activity, but positively with the apoC-III content of VLDL. Additionally, apoC-III in VLDL was associated with a higher proportion of HCV-RNA than was IgG.. ...
Jianglin Fan is the author of this article in the Journal of Visualized Experiments: Production of Apolipoprotein C-III Knockout Rabbits using Zinc Finger Nucleases
The authors of the following article have requested that it be retracted from publication in Circulation Research:. Kawakami A, Osaka M, Aikawa M, Uematsu S, Akira S, Libby P, Shimokado K, Sacks FM, Yoshida M. Toll-like receptor 2 mediates apolipoprotein CIII-induced monocyte activation. Circ Res. 2008;103:1402-1409.. The corresponding author, Dr Akio Kawakami, admitted to the editors to improperly handling the collection and presentation of data in this article such that the authors can no longer verify the authenticity and accuracy of the data presented. These errors include, but may not be limited to, the blots in Figure 2A, Figure 4D, and Online Figure III originating from unrelated experiments of the corresponding author, and the incorrect reporting of "n" in Figures 5 and 6, which are less than indicated. As such, data in those figures are not verifiable.. All co-authors involved in this study other than the corresponding author, Dr Kawakami, had no knowledge of any scientific impropriety ...
Rabbit polyclonal Apolipoprotein CIII antibody validated for WB, ELISA, ICC/IF, sELISA and tested in Human. Referenced in 3 publications. Immunogen…
Transcriptionally controlled transcription factor. Binds to DNA sites required for the transcription of alpha 1-antitrypsin, apolipoprotein CIII, transthyretin genes and HNF1-alpha. May be essential for development of the liver, kidney and intestine.
Ionis Pharmaceuticals, through its wholly owned subsidiary Akcea Therapeutics, is developing IONIS APOCIII LRx, a GalNAc3 conjugated antisense oligonucleotide
Added to this, both observational and genetic studies have been concordant in showing that remnant cholesterol (which includes intermediate-density lipoproteins, very-low-density lipoproteins, and chylomicron remnants, the products of the lipolytic degradation of triglyceride-rich lipoproteins produced by the liver and intestine) is causal for ischaemic heart disease 8. Genetic studies have also shown associations between different players in triglyceride metabolism, apolipoprotein CIII and the angiopoietins-like 3 and 4 (ANGPTL3, ANGPTL4) and coronary artery disease (9-11); the latest Focus report discusses recent data for ANGPTL3 inhibition. Moreover, given the pivotal role of peroxisome proliferator-activated receptor ? (PPAR?) in controlling the expression of a number of key genes in triglyceride and HDL metabolism, efforts have been directed to modulating the unique receptor-cofactor binding profile to improve the potency and selectivity of PPAR? ligands (the SPPARM? concept). The ...
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WELCOME to the 103rd Season of the TOK-cok, SING-song, FOOD-Loving, BBB-spreading & Cat-Loving thread! Earlier threads - EXPOSE yourself - I EXPOSE yourself - II EXPOSE yourself - III EXPOSE yourself - IV EXPOSE yourself - V EXPOSE yourself - VI
Another substance class on the rise in cardiovascular medicine are so-called anti-sense oligonucleotides, single strands of DNA or RNA binding complementary to a chosen mRNA sequence, thereby preventing protein translation. Besides a fascinating novel anti-coagulatory approach by inhibiting coagulation factor XI production, the biggest focus of this novel therapeutic approach lies on lipidology. Within this review we will highlight the current evidence on antisense therapy against apolipoprotein B, apolipoprotein A as well as apolipoprotein CIII, that are in very different stages of development, however, with some exciting early data.. Kurzfassung: Biologika begr nden eine neue Medikamentenklasse, werden biotechnologisch hergestellt und greifen gezielt in molekularbiologische Mechanismen ein. Lange Zeit eine Dom ne der H matologie, Onkologie sowie der Rheumatologie, treten monoklonale Antik rper als Therapeutika nun auch langsam in der Kardiologie ihren Siegeszug an. Neben dem schon seit mehr ...
The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details ...
View Ldlr/Ldlr Tg(APOC3)3707Bres/? involves: 129S7/SvEvBrd * C57BL/6J * CBA/J: phenotypes, images, diseases, and references.
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Distribution of apolipoprotein C-II mRNA and protein in the perinatal mouse lung. Mouse tissue sections are from saccular stage (A, B, H, GD 19.5; C, G, PN 0; I
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UCL Discovery is UCLs open access repository, showcasing and providing access to UCL research outputs from all UCL disciplines.
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Apolipoproteins function as structural components of lipoprotein particles, cofactors for enzymes, and ligands for cell-surface receptors. Most of the apoliporoteins exhibit proteoforms, arising from single nucleotide polymorphisms (SNPs) and post-translational modifications such as glycosylation, oxidation, and sequence truncations. Reviewed here are recent studies correlating apolipoproteins proteoforms with the specific clinical measures of lipid metabolism and cardiometabolic risk. Targeted mass spectrometric immunoassays toward apolipoproteins A-I, A-II, and C-III were applied on large cross-sectional and longitudinal clinical cohorts. Several correlations were observed, including greater apolipoprotein A-I and A-II oxidation in patients with diabetes and cardiovascular disease, and a divergent apoC-III proteoforms association with plasma triglycerides, indicating significant differences in the metabolism of the individual apoC-III proteoforms. These are the first studies of their kind, correlating
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Mar 7, 2005. rich lipoproteins secreted from doxycycline-treated cells was larger. cept that these two key apolipoproteins may interact within the
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Apolipoprotein (apolipoprotein) je bílkovinná složka lipoproteinů. Apolipoproteinů existuje více druhů a jednotlivé typy se vyskytují v konkrétních lipoproteinech. Apolipoproteiny mají více funkcí, jsou strukturálně důležité, pomáhají transportu lipoproteinových částic, a dokonce mohou fungovat jako koenzymy některých enzymů ...
Aim: There remains high unmet medical need for therapies to treat cardio/metabolic diseases. We validated in human trials, a platform for reducing the synthesis of genes expressed in the liver. The platform utilizes a GalNAc ligand attached to the 3 end of the sense strand of an RNAi molecule to enable delivery specifically to the liver. Here we extend the platform to targets of interest in cardiovascular disease, including PCSK9, ANGPLT3 and ApoC3.. METHODS: Chemically modified siRNAs were designed and were screened for potency in vitro. pM active siRNA molecules were developed targeting PCSK9, ANGPLT3 and ApoC3. The siRNAs were tested in either rodents or in non-human primates (NHPs) for activity.. RESULTS: In NHPs a single dose of ALN-PCSsc at 6 mg/kg reduced PCSK9 levels up to 97% and LDL-C up to 67%. Moreover the nadir effect (without any rebound of LDL-C) lasted ,30 days indicating that once a month or longer dosing frequency in clinic should be supported. Multidose studies in NHP at ...
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Hypertriglyceridemia is characterised by high levels of triglycerides in the blood and is associated with several metabolic disorders and with an increased risk of cardiovascular disease. It can be caused by several factors, including obesity, excessive alcohol consumption and an unhealthy diet. In addition, individuals with genetic defects in apolipoprotein-CII (APOC2; an activator of lipoprotein lipase, which hydrolyses triglycerides to deliver fatty acids to body tissues) display hypertriglyceridemia even on a normal diet. Here, Yury Miller and colleagues generated mutant zebrafish bearing apoc2 loss-of-function mutations. These animals, fed a normal diet, exhibit severe hypertriglyceridemia and accumulate lipid and lipid-laden macrophages in the vasculature, which constitute early events in the development of human atherosclerotic lesions. Notably, injection of wild-type zebrafish plasma with functional Apoc2 or a human APOC2-mimetic peptide can rescue hypertriglyceridemia in the mutants. ...
The impact of the common alleles at structural loci coding for apolipoprotein (apos) A-IV, E, and H on 12 quantitative risk factors for cardiovascular disease (apos A-I, A-II, B, C-II, C-III, and E; total cholesterol; triglycerides; high density lipoprotein cholesterol; systolic blood pressure; diastolic blood pressure; and red blood cell sodium-lithium countertransport) was estimated in 453 unrelated individuals (227 men and 226 women) aged 26-63 years from the Rochester Family Heart Study, who were not using medications affecting lipid levels or blood pressure. Each risk factor was adjusted for concomitants (assay date, age, age, squared, height, weight and smoking status) before the genotypic effects on mean levels and variances were estimated. Allele frequencies were the same in men and women and were similar to those observed in other studies of US Caucasians. There were very different gender-specific estimates of the relative contribution of concomitants, measured genetic effects, and ...
Plasma triglyceride levels have been correlated with insulin levels in both normal populations and in patients with endogenous hypertriglyceridemia (1). As a result of this reproducible significant association, it has been suggested that hyperinsulinism might be causally related to endogenous hypertriglyceridemia (2).. It has now been established that "endogenous hypertriglyceridemia" describes a heterogenous group of primary familial and sporadic disorders. Recently two common forms of monogenic hypertriglyceridemia have been described: "pure" monogenic familial hypertriglyceridemia, in which the hypertriglyceridemic propositus comes from a family in which all affected relatives have isolated hypertriglyceridemia; and familial combined hyperlipidemia, in which the hypertriglyceridemic propositus ...
Apolipoproteins have important structural and functional roles in several lipoprotein particles. Apolipoproteins regulate lipid metabolism, adipose tissue, and energy production and serve major...
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Apolipoprotein F山羊多克隆抗体(ab81908)可与人样本反应并经WB, ELISA, ICC实验严格验证。所有产品均提供质保服务,中国75%以上现货。
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Fructose consumption can lead to marked increases in plasma triglycerides in both humans and laboratory animals. We have observed that overnight access to a 16% fructose solution can promote hypertriglyceridemia in rats. Several investigators have suggested that APOC 3 may be implicated in promoting fructose-induced hypertriglyceridemia. We have examined the role of APOC 3 in liver and blood taken from rats that had been given access to a fructose solution overnight as a supplement to standard laboratory chow. Hepatic APOC3 mRNA expression from fructose alone resulted in a 14 % reduction compared to control. Interestingly, hepatic APOC3 expression was increased by about 250% in sucrose, high fructose corn syrup and glucose groups. The serum protein levels of APOC3 did not differ across groups. Contrary to our hypothesis, these results indicate that glucose containing sugars increased hepatic APOC3 mRNA expression but no sugar was capable of increasing the serum protein level.
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This gene encodes a member of the apolipoprotein C1 family. This gene is expressed primarily in the liver, and it is activated when monocytes differentiate into macrophages. The encoded protein plays a central role in high density lipoprotein (HDL) and very low density lipoprotein (VLDL) metabolism. This protein has also been shown to inhibit cholesteryl ester transfer protein in plasma. A pseudogene of this gene is located 4 kb downstream in the same orientation, on the same chromosome. This gene is mapped to chromosome 19, where it resides within a apolipoprotein gene cluster. Alternative splicing and the use of alternative promoters results in multiple transcript variants. [provided by RefSeq, Sep 2016 ...
To test whether triglyceride-enriched low-density lipoprotein (LDL) obtained from subjects with diabetic hypertriglyceridemia is metabolized normally by cells, LDL was separated from seven healthy control subjects (fasting plasma glucose [FPG] 91 ± 10 mg/dl [mean ± SD], triglyceride [TG] 110 ± 47 mg/dl), six diabetic normolipidemic patients (FPG 218 ± 65 mg/dl; TG 139 ± 75 mg/dl), six diabetic hypertriglyceridemic patients (FPG 214 ± 71 mg/dl; TG 1915 ± 1680 mg/dl), and five nondiabetic hypertriglyceridemic patients (FPG 92 ± 8 mg/dl; TG 2013 ± 1889 mg/dl). Binding of 125l-labeled LDL from hypertriglyceridemic subjects with and without diabetes to cultured skin fibroblasts was significantly decreased to 74 ± 19% and 78 ± 14% of that seen with LDL from normolipidemic nondiabetic subjects and diabetic normolipidemic controls (100 ± 0%, 101 ± 25%; P , 0.005). Unlabeled LDL from hypertriglyceridemic subjects with and without diabetes failed to suppress LDL receptor activity and sterol ...
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Hypertriglyceridemia (HTG) is commonly encountered in lipid and cardiology clinics. Severe HTG warrants treatment because of the associated increased risk of acute pancreatitis. However, the need to treat, and the correct treatment approach for patients with mild to moderate HTG are issues for ongoing evaluation. In the past, it was felt that triglyceride does not directly contribute to development of atherosclerotic plaques. However, this view is evolving, especially for triglyceride-related fractions and variables measured in the non-fasting state. Our understanding of the etiology, genetics and classification of HTG states is also evolving. Previously, HTG was considered to be a dominant disorder associated with variation within a single gene. The old nomenclature includes the term
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Apolipoprotein A-II is a protein that in humans is encoded by the APOA2 gene. This gene encodes apolipoprotein (apo-) A-II, ... "Entrez Gene: APOA2 apolipoprotein A-II". Pussinen PJ, Jauhiainen M, Metso J, Pyle LE, Marcel YL, Fidge NH, Ehnholm C (Jan 1998 ... Brewer HB, Lux SE, Ronan R, John KM (May 1972). "Amino acid sequence of human apoLp-Gln-II (apoA-II), an apolipoprotein ... The protein is found in plasma as a monomer, homodimer, or heterodimer with apolipoprotein D. Defects in this gene may result ...
Apolipoprotein L3 is a protein that in humans is encoded by the APOL3 gene. This gene is a member of the apolipoprotein L gene ... Six transcript variants encoding three different isoforms have been found for this gene. GRCh38: Ensembl release 89: ... "Entrez Gene: APOL3 apolipoprotein L, 3". Human APOL3 genome location and APOL3 gene details page in the UCSC Genome Browser. ... 2001). "Apolipoprotein L gene family: tissue-specific expression, splicing, promoter regions; discovery of a new gene". J. ...
Apolipoprotein L2 is a protein that in humans is encoded by the APOL2 gene. This gene is a member of the apolipoprotein L gene ... "Entrez Gene: APOL2 apolipoprotein L, 2". Human APOL2 genome location and APOL2 gene details page in the UCSC Genome Browser. ... McGhee KA, Morris DW, Schwaiger S (2005). "Investigation of the apolipoprotein-L (APOL) gene family and schizophrenia using a ... Monajemi H, Fontijn RD, Pannekoek H, Horrevoets AJ (2002). "The apolipoprotein L gene cluster has emerged recently in evolution ...
Apolipoprotein L6 is a protein that in humans is encoded by the APOL6 gene. This gene is a member of the apolipoprotein L gene ... "Entrez Gene: APOL6 apolipoprotein L, 6". Human APOL6 genome location and APOL6 gene details page in the UCSC Genome Browser. ... Liu Z, Lu H, Jiang Z, Pastuszyn A, Hu CA (Jan 2005). "Apolipoprotein l6, a novel proapoptotic Bcl-2 homology 3-only protein, ... "The human apolipoprotein L gene cluster: identification, classification, and sites of distribution". Genomics. 74 (1): 71-8. ...
Apolipoprotein E (ApoE) plays an important role in phospholipid and cholesterol homeostasis. After binding ApoER2, ApoE is ... It is separated into a ligand binding domain of eight ligand binding regions, an EGF-like domain containing three cysteine-rich ... Riddell DR, Sun XM, Stannard AK, Soutar AK, Owen JS (2001). "Localization of apolipoprotein E receptor 2 to caveolae in the ... Herz J (June 2009). "Apolipoprotein E receptors in the nervous system". Curr. Opin. Lipidol. 20 (3): 190-6. doi:10.1097/MOL. ...
Sacks FM, Zheng C, Cohn JS (2011). "Complexities of plasma apolipoprotein C-III metabolism". Journal of Lipid Research. 52 (6 ... Its most abundant apolipoproteins are apo A-I and apo A-II. A rare genetic variant, ApoA-1 Milano, has been documented to be ... In the stress response, serum amyloid A, which is one of the acute-phase proteins and an apolipoprotein, is under the ... They are typically composed of 80-100 proteins per particle (organized by one, two or three ApoA; more as the particles enlarge ...
Katan MB (March 1986). "Apolipoprotein E isoforms, serum cholesterol, and cancer". Lancet. 1 (8479): 507-8. PMID 2869248. Gray ... 288 (3): 321-33. doi:10.1001/jama.288.3.321. PMID 12117397. Fisher RA (April 2010). "Statistical methods in genetics. 1951". ... 7 Suppl 3: 9-12. PMID 1855097. Smith GD (September 2010). "Mendelian Randomization for Strengthening Causal Inference in ...
August 1992). "Apolipoprotein AI mutation Arg-60 causes autosomal dominant amyloidosis". Proc. Natl. Acad. Sci. U.S.A. 89 (16 ... with congenital mutations in apolipoprotein A1 and lysozyme. It is also known as "Ostertag" type, after B. Ostertag, who ... 118 (3): 321-2. doi:10.1016/j.amjmed.2004.10.022. PMID 15745733. Granel B, Valleix S, Serratrice J, et al. (January 2006). " ... 5 (3): 188-92. doi:10.3109/13506129809003844. PMID 9818055. Soutar AK, Hawkins PN, Vigushin DM, et al. ( ...
... or apolipoprotein C-II is a protein that in humans is encoded by the APOC2 gene. secreted in plasma where it ... "A nonsense mutation in the apolipoprotein C-IIPadova gene in a patient with apolipoprotein C-II deficiency". J. Clin. Invest. ... Familial apolipoprotein CII deficiency associated with premature vascular disease". J. Clin. Invest. 80 (6): 1597-606. doi: ... "Structure of apolipoprotein C-IIToronto, a nonfunctional human apolipoprotein". Proc. Natl. Acad. Sci. U.S.A. 84 (1): 270-3. ...
... although nonglycosylated and immature forms of apolipoprotein[a] are competent to associate with apolipoprotein B-100 in vitro ... The half-life of Lp(a) in the circulation is approximately three to four days. The mechanism and sites of Lp(a) catabolism are ... although nonglycosylated and immature forms of apolipoprotein[a] are competent to associate with apolipoprotein B-100 in vitro ... III. Contribution of Lp(a) glycoprotein phenotypes to normal lipid variation". Hum. Genet. 82 (1): 73-8. doi:10.1007/BF00288277 ...
Apolipoprotein B48 on chylomicra and Apolipoprotein B100 on LDL, IDL, and VLDL are important for MTP binding. Click on genes, ... Gordon DA (1997). "Recent advances in elucidating the role of the microsomal triaglyceride transfer protein in apolipoprotein B ... 1999). "A common binding site on the microsomal triaglyceride transfer protein for apolipoprotein B and protein disulfide ... The network of endoplasmic reticulum-resident chaperones (ERp72, GRP94, calreticulin, and BiP) interacts with apolipoprotein b ...
Apolipoprotein E, dementia, and cortical deposition of beta-amyloid protein. „N Engl J Med". 333 (19), s. 1242-47, 11 1995. DOI ... Następcze badania kliniczne III fazy nie dały jednak pozytywnych efektów, zarówno w przypadku pierwotnych, jak i wtórnych ... Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial ... a b Mahley RW, Weisgraber KH, Huang Y. Apolipoprotein E4: A causative factor and therapeutic target in neuropathology, ...
Basu SK, Goldstein JL, Brown MS (Feb 1983). "Independent pathways for secretion of cholesterol and apolipoprotein E by ... 41 (3): 735-43. doi:10.1016/S0092-8674(85)80054-4. PMID 3924410. Osborne TF, Goldstein JL, Brown MS (Aug 1985). "5' end of HMG ... 65 (3): 429-34. doi:10.1016/0092-8674(91)90460-G. PMID 2018975. Chen WJ, Andres DA, Goldstein JL, Russell DW, Brown MS (Jul ... 89 (3): 331-40. doi:10.1016/S0092-8674(00)80213-5. PMID 9150132. DeBose-Boyd RA, Brown MS, Li WP, Nohturfft A, Goldstein JL, ...
All members of this family are receptors for Apolipoprotein E (ApoE). Therefore, they are often synonymously referred to as ' ... This fragment may serve postnatally to prevent apical dendrites of cortical layer II/III pyramidal neurons from overgrowth, ... Andersen OM, Benhayon D, Curran T, Willnow TE (Aug 2003). "Differential binding of ligands to the apolipoprotein E receptor 2 ... Herz J, Beffert U (Oct 2000). "Apolipoprotein E receptors: linking brain development and Alzheimer's disease". Nature Reviews. ...
Takahashi K, Ikeo K, Gojobori T (1991). "Evolutionary origin of numerous kringles in human and simian apolipoprotein(a)". FEBS ... Kringle domains have been found in plasminogen, hepatocyte growth factors, prothrombin, and apolipoprotein(a). Kringles are ... 212 (3): 541-552. doi:10.1016/0022-2836(90)90330-O. PMID 2157850. Castellino FJ, Beals JM (1987). "The genetic relationships ... Kringle domains are characterised by a triple loop, 3-disulfide bridge structure, whose conformation is defined by a number of ...
... and involves apolipoprotein A1. "FAP-IV" is also known as "Finnish-type", and involves gelsolin. Fibrinogen, apolipoprotein A1 ... Senile systemic amyloidosis [abbreviated "SSA"] is also associated with transthyretin aggregation.) "FAP-III" is also known as ... These proteins include: transthyretin (ATTR, the most commonly implicated protein), apolipoprotein A1, and gelsolin. Due to the ... 75 (3): 408-27. doi:10.1093/brain/75.3.408. PMID 12978172. Kelly JW (February 1996). "Alternative conformations of ...
"Deficiency of glycine N-methyltransferase aggravates atherosclerosis in apolipoprotein E-null mice". Molecular Medicine. 18: ... 87: 132-3. doi:10.1016/j.jprot.2013.01.007. PMID 23340451. Chen CY, Ching LC, Liao YJ, Yu YB, Tsou CY, Shyue SK, Chen YM, Lee ... 235 (3): 296-304. doi:10.1016/j.taap.2008.12.013. PMID 19146867. Chen YM, Shiu JY, Tzeng SJ, Shih LS, Chen YJ, Lui WY, Chen PH ... 29 (3): 494-501. doi:10.1111/jgh.12434. PMID 24219143. Wang YC, Lin WL, Lin YJ, Tang FY, Chen YM, Chiang EP (February 2014). "A ...
Zhang J, Herscovitz H (February 2003). "Nascent lipidated apolipoprotein B is transported to the Golgi as an incompletely ... Linnik KM, Herscovitz H (August 1998). "Multiple molecular chaperones interact with apolipoprotein B during its maturation. The ... Calcitonin receptor has been shown to interact with Apolipoprotein B and LRP1. GRCh38: Ensembl release 89: ENSG00000004948 - ... 458 (3): 409-14. doi:10.1016/S0014-5793(99)01176-X. PMID 10570950. Beaudreuil J, Taboulet J, Orcel P, Graulet AM, Denne MA, ...
Class III: LDLR does not properly bind LDL on the cell surface because of a defect in either apolipoprotein B100 (R3500Q) or in ... Apolipoprotein B, in its ApoB100 form, is the main apolipoprotein, or protein part of the lipoprotein particle. Its gene is ... In January 2013, The US FDA also approved mipomersen, which inhibits the action of the gene apolipoprotein B, for the treatment ... LDL cholesterol normally circulates in the body for 2.5 days, and subsequently the apolipoprotein B portion of LDL cholesterol ...
"Entrez Gene: APOBEC3C apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3C". Yu Q, Chen D, König R, Mariani R, ... 457 (3): 295-9. doi:10.1016/j.bbrc.2014.12.103. PMID 25576866. Yu Q, König R, Pillai S, Chiles K, Kearney M, Palmer S, Richman ... 8 (3): 148-57. PMID 17078485. Madsen P, Anant S, Rasmussen HH, Gromov P, Vorum H, Dumanski JP, Tommerup N, Collins JE, Wright ... 94 (1-3): 203-8. doi:10.1016/j.jsbmb.2005.01.007. PMID 15862967. Doehle BP, Schäfer A, Wiegand HL, Bogerd HP, Cullen BR (July ...
Three later studies failed to support that finding. It may also be necessary to take into consideration that absorption of ... Taurine has been shown to reduce the secretion of apolipoprotein B100 and lipids in HepG2 cells. High concentrations of serum ... Yanagita, T; Han, SY; Hu, Y; Nagao, K; Kitajima, H; Murakami, S (2008). "Taurine reduces the secretion of apolipoprotein B100 ... 2006). "Effects of taurine on rat behaviors in three anxiety models". Pharmacol. Biochem. Behav. 83 (2): 271-6. doi:10.1016/j. ...
Ichinose A (1992). "Multiple members of the plasminogen-apolipoprotein(a) gene family associated with thrombosis". Biochemistry ... 4 (3): 449-51. doi:10.1016/0888-7543(89)90356-X. PMID 2714803. Magnaghi P, Citterio E, Malgaretti N, et al. (1994). "Molecular ... 3 (3): 437-42. doi:10.1093/hmg/3.3.437. PMID 8012354. Kida M, Wakabayashi S, Ichinose A (1997). "Characterization of the 5'- ... 259 (3): 618-25. doi:10.1046/j.1432-1327.1999.00055.x. PMID 10092845. Strausberg RL, Feingold EA, Grouse LH, et al. (2003). " ...
... cause cerebrotendinous xanthomatosis in three Japanese patients from two unrelated families". Journal of Lipid Research. 38 (5 ... "Overexpression of steroidogenic acute regulatory protein increases macrophage cholesterol efflux to apolipoprotein AI". ... 61 (3): 185-91. doi:10.1034/j.1399-0004.2002.610303.x. PMID 12000359. Björkhem I, Araya Z, Rudling M, Angelin B, Einarsson C, ... 86 (3): 526-34. doi:10.1093/cvr/cvq015. PMID 20083572. Mast N, Lin JB, Pikuleva IA (September 2015). "Marketed Drugs Can ...
"Entrez Gene: APOBEC3D apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3D (putative)". Human APOBEC3D genome ...
April 1987). "Association of an apolipoprotein CII allele with familial dementia of the Alzheimer type". Journal of ... 4 (2-3): 97-108. doi:10.3109/01677068709102337. PMID 2885403. Martin GM (1971). "Brief proposal on immortality: an interim ...
It contains three exons that span more than 5 kb of genomic DNA, and it encodes a fucosyltransferase that produces the H ... Apolipoprotein E, gene associated with Alzheimer's disease. Gene map locus 19q13.2 CIC: Capicua transcriptional repressor. Gene ... 64 (3): 189-196. doi:10.1046/j.1469-1809.2000.6430189.x. PMC 3376086 . PMID 11409409. Dean, L. (2005). "Ch. 5: The ABO blood ... ISBN 978-3-318-02253-7. Sethakulvichai, W.; Manitpornsut, S.; Wiboonrat, M.; Lilakiatsakun, W.; Assawamakin, A.; Tongsima, S. ( ...
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"The antioxidant N-acetylcysteine prevents accelerated atherosclerosis in uremic apolipoprotein E knockout mice". Kidney ... 50 (3): 341-51. doi:10.1177/002215540205000306. PMID 11850437. Pacher P, Obrosova IG, Mabley JG, Szabó C (2005). "Role of ... 12 (3): 267-75. doi:10.2174/0929867053363207. PMC 2225483 . PMID 15723618. Ivanovski O, Szumilak D, Nguyen-Khoa T, Ruellan N, ... 3-Nitro-L-tyrosine at Sigma-Aldrich Ischiropoulos H (August 1998). "Biological tyrosine nitration: a pathophysiological ...
Biophysical analysis of apolipoprotein E3 variants linked with development of type III hyperlipoproteinemia.. Georgiadou D1, ... Biophysical Analysis of Apolipoprotein E3 Variants Linked with Development of Type III Hyperlipoproteinemia ... Biophysical Analysis of Apolipoprotein E3 Variants Linked with Development of Type III Hyperlipoproteinemia ... Biophysical Analysis of Apolipoprotein E3 Variants Linked with Development of Type III Hyperlipoproteinemia ...
Clinical mass spectrometry test for apolipoprotein C-III proteoforms. Printer-friendly version ... The new apolipoprotein C III MS test will transform clinical research by enabling fast and cost effective screening of apoC III ... translationOur recent studies have revealed strong associations between relative abundance of a specific apolipoprotein C III ... lipid metabolism and cardiometabolic riskWe propose to develop and demonstrate a low costhigh throughput MALDI TOF MS apoC III ...
Production of Apolipoprotein C-III Knockout Rabbits using Zinc Finger Nucleases. Dongshan Yang1, Jifeng Zhang1, Jie Xu1, ... Apolipoprotein (Apo) C-III (ApoCIII) is a small O-glycosylated secretory protein that is synthesized mainly in the liver and ... Apolipoprotein (Apo) C-III (ApoCIII) resides on the surface of plasma chylomicron (CM), very low density lipoprotein (VLDL) and ... Yang, D., Zhang, J., Xu, J., Zhu, T., Fan, Y., Fan, J., Chen, Y. E. Production of Apolipoprotein C-III Knockout Rabbits using ...
Isoelectric focusing resolves apoC-III into three isoforms: apoC-III0, apoC-III1, and apoC-III2. ApoC-III1 was investigated in ... Apolipoprotein (apo)-C-III is an 8.8-kDa glycoprotein synthesized by the liver and intestines. ApoC-III is highly associated ... Both VLDL apoC-III FCR and PR were independent determinants of VLDL apoC-III concentration. The increase in VLDL apoC-III FCR ... Plasma apolipoprotein C-III transport in central obese men: associations with very-low density lipoprotein apolipoprotein B and ...
2015 May-Jun;9(3):360-7. doi: 10.1016/j.jacl.2014.12.001. Epub 2014 Dec 11. Randomized Controlled Trial; Research Support, N.I. ... apoB and apoC-III were significantly decreased by the high dose relative to placebo and low dose (P , .01), as was very low- ... The high- and low-dose effects differed significantly for heparin-precipitated apoC-III, LpB, LpA-I, and apoB/apoA-I ratio (P ... The effects of 3.4 g/d EPA + DHA on apoB and apoC-III may reduce atherosclerotic plaque progression in individuals with ...
Yu Du, Li Wang, Shuyi Si, Yuan Yang, Bin Hong, A novel compound 4010B-30 upregulates apolipoprotein A-I gene expression through ... To identify the mechanisms by which cocoa induces HDL levels and since apolipoprotein AI (ApoAI) is the major protein in HDLs, ... and NFY-mediated transcription of apolipoprotein AI in human cells. Authors. *. Carlota Oleaga,. *Department of Biochemistry ... 3. Torsten Bohn, Gordon J. McDougall, Amparo Alegría, Marie Alminger, Eva Arrigoni, Anna-Marja Aura, Catarina Brito, Antonio ...
Do Apolipoprotein E Polymorphisms Influence Risk of Cognitive Decline by Modulating Omega-3 Fatty Acid Metabolism?. The safety ... Do Apolipoprotein E Polymorphisms Influence Risk of Cognitive Decline by Modulating Omega-3 Fatty Acid Metabolism?. ... ii) 13C-DHA metabolism changes while on a dietary supplement of EPA+DHA; iii) Better cognitive performance occurs while on EPA+ ... the epsilon 4 allele of apolipoprotein E (ApoE4) is associated with twice the prevalence of late-onset Alzheimers disease (AD ...
Chemicals/CAS: apolipoprotein E3 (Leidein); Apolipoprotein E3; Apolipoproteins E; Bile Acids and Salts; cafestol, 469-83-0; ... Biology · Animals · Apolipoprotein E3 · Apolipoproteins E · Bile Acids and Salts · Cholesterol · Diet · Diterpenes · Feces · ... Cafestol increases serum cholesterol levels in apolipoprotein E*3- leiden transgenic mice by suppression of bile acid synthesis ... In apoE*3-Leiden mice, serum cholesterol was statistically significantly increased by 33% on the low- and by 61% on the high- ...
Low-density lipoprotein (LDL) that contains apolipoprotein (apo) C-III makes up only 10% to 20% of plasma LDL but has a ... "Low-Density Lipoproteins Containing Apolipoprotein C-III and the Risk of Coronary Heart Disease." Circulation 124 (19) (October ... Low-Density Lipoproteins Containing Apolipoprotein C-III and the Risk of Coronary Heart Disease. ... the relative risks for the top versus bottom quintile of LDL with apoC-III were greater than those for LDL without apoC-III. ...
To assess the consequences of epilepsy and APOE genotype on neurons, we counted neurons in cortical layers III to VI of three ... Three images per slide (40X magnification) were captured at identical exposure settings, using a Nikon Eclipse E600 microscope ... Liu L, Aboud O, Jones RA, Mrak RE, Griffin ST, Barger SW: Apolipoprotein E expression is elevated by interleukin 1 and other ... Marz W, Scharnagl H, Kirca M, Bohl J, Gross W, Ohm TG: Apolipoprotein E polymorphism is associated with both senile plaque load ...
Background: Apolipoprotein C-III (apoC-III) inhibits lipoprotein lipase activity and hepatic uptake of triglyceride-rich ... Abstract 19030: Apolipoprotein C-III is Significantly Reduced by Prescription Omega-3 Free Fatty Acids (Epanova) in Patients ... Abstract 19030: Apolipoprotein C-III is Significantly Reduced by Prescription Omega-3 Free Fatty Acids (Epanova) in Patients ... Abstract 19030: Apolipoprotein C-III is Significantly Reduced by Prescription Omega-3 Free Fatty Acids (Epanova) in Patients ...
... Meyers, Nathan L. ... ApoC-III elevates TG in part by inhibiting LPL. ApoC-III likely inhibits LPL by competing for lipid binding. To probe this, we ... ApoC-III adsorption increased surface pressure by upward of 18 mN/m at phospholipid/TG/water interfaces. ApoC-III was retained ... Increased apoC-III expression in the hypertriglyceridemic state allows apoC-III to accumulate on lipoproteins and inhibit LPL ...
Scavenger receptor function of mouse Fcγ receptor III contributes to progression of atherosclerosis in apolipoprotein E ... In this report, we show that apolipoprotein E (apoE)-CD16 double knockout (DKO; apoE-CD16 DKO) mice have reduced ...
ApoC-III1 and apoC-III2 are the most abundant C-III apolipoproteins in human plasma compared with apoC-III0. Given that apoC- ... Apolipoproteins C-III and A-V as Predictors of Very-Low-Density Lipoprotein Triglyceride and Apolipoprotein B-100 Kinetics. ... Apolipoproteins C-III and A-V as Predictors of Very-Low-Density Lipoprotein Triglyceride and Apolipoprotein B-100 Kinetics ... Apolipoproteins C-III and A-V as Predictors of Very-Low-Density Lipoprotein Triglyceride and Apolipoprotein B-100 Kinetics ...
The American Heart Association is a qualified 501(c)(3) tax-exempt organization.. *Red Dress™ DHHS, Go Red™ AHA; National Wear ... Endogenously Decreasing Tissue n-6/n-3 Fatty Acid Ratio Reduces Atherosclerotic Lesions in Apolipoprotein E-Deficient Mice by ... Endogenously Decreasing Tissue n-6/n-3 Fatty Acid Ratio Reduces Atherosclerotic Lesions in Apolipoprotein E-Deficient Mice by ... Endogenously Decreasing Tissue n-6/n-3 Fatty Acid Ratio Reduces Atherosclerotic Lesions in Apolipoprotein E-Deficient Mice by ...
Serum amyloid A, apolipoprotein C (apoC-III) and apolipoprotein A-II (apoA-II) were selected to confirm the proteomics results ... Lv, P., Zhao, M., Liu, Y., Jin, H., Cui, W., Fan, C., Teng, Y., Zheng, L., Huang, Y.Apolipoprotein C-III in the high-density ... Lv, P., Zhao, M., Liu, Y., Jin, H., Cui, W., Fan, C., Teng, Y., Zheng, L., Huang, Y.Apolipoprotein C-III in the high-density ... Apolipoprotein C-III in the high-density lipoprotein proteome of cerebral lacunar infarction patients impairs its anti- ...
Knockdown of hMDM apoE inhibited basal cholesterol efflux by 20% without altering apolipoprotein-AI mediated cholesterol efflux ... Apolipoprotein-E (apoE) expression may be associated with apoptosis resistance. Since macrophages constitutively synthesize ... In these experiments, staurosporine-induced caspase-3 activation was increased by 49% in apoE null compared to wild type mBMDM ... In conclusion, apoE expression modulates capase-3 activity, but this has no significant impact on sensitivity to apoptosis and ...
Apolipoprotein C-III (apoC-III) is a key regulator of lipoprotein metabolism. We investigated whether subspecies of HDL defined ... High-Density Lipoprotein Subspecies Defined by Presence of Apolipoprotein C-III and Incident Coronary Heart Disease in Four ... ApoC-III was found on 6% to 8% of apoA-I. The 2 HDL subspecies showed opposing associations, with risk of CHD in each of the ... Our findings from 4 prospective studies support the hypothesis that apoC-III may mark a subfraction of HDL that is associated ...
Type III hyperlipoproteinemia (HLP) is a genetic disorder of lipid metabolism in humans in which the primary molecular defect ... is a mutation(s) in apolipoprotein (apo) E that causes defective... ... The Apolipoprotein E Cys-142 Mutant: Role in Dominant Inheritance of Type III Hyperlipoproteinemia and Expression in Transgenic ... In: Sirtori C.R., Franceschini G., Brewer B.H. (eds) Human Apolipoprotein Mutants III. NATO ASI Series (Series H: Cell Biology ...
Modulation of hepatic apolipoprotein B, 3-hydroxy-3-methylglutaryl-CoA reductase and low-density lipoprotein receptor mRNA and ... Modulation of hepatic apolipoprotein B, 3-hydroxy-3-methylglutaryl-CoA reductase and low-density lipoprotein receptor mRNA and ... Modulation of hepatic apolipoprotein B, 3-hydroxy-3-methylglutaryl-CoA reductase and low-density lipoprotein receptor mRNA and ... Modulation of hepatic apolipoprotein B, 3-hydroxy-3-methylglutaryl-CoA reductase and low-density lipoprotein receptor mRNA and ...
Overproduction of intestinal lipoprotein containing apolipoprotein B-48 in: impact of dietaryn-3 fatty acidsPsammomys obesus: ... fish oil feeding resulted in diminished triglyceride-rich lipoprotein assembly and apolipoprotein (apo) B-48 biogenesis, ... Our data highlight the beneficial impact of n-3 fatty acids on adverse effects of the metabolic syndrome and emphasise their ... We therefore tested the hypothesis that n-3 fatty acids improve the various events governing intra-enterocyte lipid transport ...
... multiphoton microscopy for three-dimensional imaging of lymphocyte recruitment into apolipoprotein-E-deficient mouse carotid ... multiphoton microscopy for three-dimensional imaging of lymphocyte recruitment into apolipoprotein-E-deficient mouse carotid ... Two recent elegant studies have shown that in apolipoprotein-E- deficient mice, the lamina adventitia is a major site of ...
Effects of omega-3 fatty acid supplements on serum lipids, apolipoproteins and malondialdehyde in type 2 diabetes patients ... apolipoprotein B-100 (Apo B-100), apolipoprotein A-I (Apo A-I), malondialdehyde (MDA) (as index for lipid peroxidation), and ... Effects of omega-3 fatty acid supplements on serum lipids, apolipoproteins and malondialdehyde in type 2 diabetes patients ... In the omega-3 fatty acid group, fasting TG decreased significantly by 31.2 % (P = 0.01) relative to the placebo group; there ...
The 4 allele of the apolipoprotein E gene (ApoE) is a genetic risk factor for late-onset AD. ApoE plays a key role in the ... The 4 allele of the apolipoprotein E gene (ApoE) is a genetic risk factor for late-onset AD. ApoE plays a key role in the ... Interaction with Apolipoprotein E Genotype. Author(s): P. Barberger-Gateau, C. Samieri, C. Feart, M. Plourde. INSERM, U897, ... Keywords: Alzheimers disease, apolipoprotein E, fatty acids, omega 3, nutrition, dementia, ApoE polymorphism, Caucasian ...
... below pre-treatment levels in all three groups. Levels of high-density lipoprotein (HDL) cholesterol and apolipoprotein A-I ... and apolipoprotein A-I 11-15% from those obtained with unopposed estrogen. The LDL cholesterol levels fell 12-19% with ... all three progestogens reversed some of the favorable effects of unopposed estrogen on lipoproteins but permitted a continued ... The effects of conjugated equine estrogen and subsequent cyclical progestogen supplementation on lipoprotein and apolipoprotein ...
  • Apolipoprotein E (apoE) is a major protein of the lipoprotein transport system that plays important roles in lipid homeostasis and protection from atherosclerosis. (nih.gov)
  • Mutations in the 136-150 region of the N-terminal domain of apoE, reduce its low density lipoprotein (LDL) receptor binding capacity and have been linked with lipoprotein disorders, such as type III hyperlipoproteinemia (HLP) in humans. (nih.gov)
  • IMPLICATIONS: This project will help explain the apparent link that is newly emerging between ApoE polymorphisms, altered omega-3 fatty acid metabolism and risk of cognitive decline, and should help in the development of nutraceutical-based clinical trials using fish oil for the elderly. (clinicaltrials.gov)
  • ApoE*3-Leiden, heterozygous low density lipoprotein-receptor (LDLR+/-) knockout, or wild-type (WT) C57BL/6 mice were fed a high- (0.05% wt/wt) or a low- (0.01% wt/wt) cafestol diet or a placebo diet for 8 weeks. (tudelft.nl)
  • In apoE*3-Leiden mice, serum cholesterol was statistically significantly increased by 33% on the low- and by 61% on the high-cafestol diet. (tudelft.nl)
  • To investigate the mechanism of this effect, apoE*3-Leiden mice were fed a high-cafestol or a placebo diet for 3 weeks. (tudelft.nl)
  • In conclusion, cafestol increases serum cholesterol levels in apoE*3-Leiden mice by suppression of the major regulatory enzymes in the bile acid synthesis pathways, leading to decreased LDLR mRNA levels and increased secretion of hepatic cholesterol esters. (tudelft.nl)
  • With an eye toward defining ways in which APOE ε3 alleles may foster neuronal well-being in epilepsy and/or APOE ε4 alleles exacerbate neuronal decline, neuronal and glial characteristics were studied in temporal lobectomy specimens from epilepsy patients of either APOE ε4,4 or APOE ε3,3 genotype. (springer.com)
  • APOE ε3,3 age 17). (springer.com)
  • Our findings of neuronal and glial events, which correlate with lesser neuronal DNA damage and larger, more robust neurons in epilepsy patients of APOE ε3,3 genotype compared to APOE ε4,4 genotype carriers, are consistent with the idea that the APOE ε 3,3 genotype better protects neurons subjected to the hyperexcitability of epilepsy and thus confers less risk of AD (Alzheimer's disease). (springer.com)
  • Type III hyperlipoproteinemia (HLP) is a genetic disorder of lipid metabolism in humans in which the primary molecular defect is a mutation(s) in apolipoprotein (apo) E that causes defective interaction of apoE with lipoprotein receptors and an accumulation of cholesterol-rich β-VLDL in the blood (Mahley and Rall, 1989). (springer.com)
  • Most often, type III HLP is associated with homozygosity for an apoE mutant that has cysteine instead of arginine at residue 158, i.e ., with recessive inheritance. (springer.com)
  • Many rare mutants of apoE have now been described (Fig. 1), some of which are also associated with type III HLP. (springer.com)
  • In most of these rare instances, type III HLP is transmitted in a dominant fashion, i.e ., heterozygosity for the apoE mutant is sufficient for expression of the disorder. (springer.com)
  • One of these rare apoE variants (cysteine instead of arginine at residue 142) has been found in a single family in which seven members spanning four generations are heterozygous for this apoE variant and all seven have type III HLP (Havel et al . (springer.com)
  • 1989). Because of the unusual nature of the disorder in this family, we undertook investigations of the properties of the apoE Cys-142 mutant to determine its role in the expression of type III HLP. (springer.com)
  • The 4 allele of the apolipoprotein E gene (ApoE) is a genetic risk factor for late-onset AD. (eurekaselect.com)
  • The action of n-3 PUFA on the aging brain might therefore differ according to ApoE polymorphism. (eurekaselect.com)
  • Apolipoprotein E, type epsilon 4 allele (ApoE epsilon 4), is associated with late-onset sporadic Alzheimer's disease (AD) in French patients. (unboundmedicine.com)
  • Although apolipoprotein E (apoE) is the most common genetic risk factor for Alzheimer's Disease (AD), how apoE participates in AD pathogenesis remains incompletely understood. (unboundmedicine.com)
  • ABCA1 catalyses the ATP-dependent transport of cholesterol and phospholipids from the plasma membrane to lipid-free apolipoproteins including apoE. (unboundmedicine.com)
  • Apolipoprotein E (APOE4) is the most important known genetic risk for AD and is prevalent in 20-25% of Canadians, but at present, knowing an individual's ApoE genotype does not help the diagnosis, treatment or prevention of AD. (clinicaltrials.gov)
  • Two distal downstream enhancers controlling astrocyte expression of the human apolipoprotein E (apoE) gene in the brain were identified by analysis of transgenic mice generated with various constructs of the apoE/C-I/C-IV/C-II gene cluster. (jneurosci.org)
  • Apolipoprotein E (apoE) is a protein ( M r = 35,000) that functions in the CNS. (jneurosci.org)
  • To test this hypothesis, we investigated the effect of repeated systemic inoculations with Porphyromonas gingivalis ( Pg ), a putative periodontal pathogen, on the progression of atherosclerosis in heterozygous apolipoprotein E-deficient (ApoE +/− ) mice. (ahajournals.org)
  • To address this question, in this study, we examine for the first time the renoprotective actions of alagebrium in diabetic RAGE apolipoprotein E ( apoE ) double-knockout (KO) mice, with a particular emphasis on glomerular fibrosis and inflammation, comparing its effects with those of the ACE inhibitor, quinapril. (diabetesjournals.org)
  • Male ApoE −/− mice (3 months old) were purchased from the Animal Resources Centre, Perth, Australia. (frontiersin.org)
  • LDL-C (-27%), lathosterol (-40%), apoB (- 22%), apoC-III (-37%), and apoE (-24%) and modestly decreased the levels of HDL-C (-12%) and apoA-I (-11%) (percent relative to the average pretreatment and posttreatment baseline values) but did not affect the levels of TG, VLDL-C, the lathosterol/TC ratio, or LCAT activity. (tudelft.nl)
  • LDL-C, apoB, apoC-III, and apoE to simvastatin in the FHC swines is similar to that observed in humans, although the drug is less potent and efficacious in swine, while the results are different from those in humans with regard to the remaining parameters. (tudelft.nl)
  • Significant association of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) rs3846662 and sirtuin 1 (SIRT1) rs7895833 and apolipoprotein E (APOE) h. (cdc.gov)
  • In addition, we also analyzed the association between APOE methylation and MCI.Forty-three MCI and 125 controls were included in the present study. (cdc.gov)
  • In humans, there are three alleles of the apoE gene (designated ε2, ε3, and ε4), encoding the respective isoforms of the protein (E2, E3, and E4) ( 19 ). (asm.org)
  • ApoE may play an important modulatory function in the central nervous system (CNS), because while in the peripheral nervous system several other apolipoproteins are involved in lipid transport, in the CNS there is less redundancy of such molecules ( 19 , 26 ). (asm.org)
  • First, it has been reported that sufferers from cold sores are more likely to carry the apoE ε4 allele than controls ( 3 ). (asm.org)
  • Objectives: To evaluate the frequency of apolipoprotein (APOE) alleles and determine whether APOE type 4 allele (e4) was associated with edentulousness even when certain factors were controlled.Background: The APOE are important in lipid homeostasis, and APOE e4 has been found in many diseases and to have a negative impact on longevity. (diva-portal.org)
  • abstract = "The nicotine-derived nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1- butanone (NNK) is one of the most potent lung carcinogens in rodents. (elsevier.com)
  • 4 proteins (complement factor H, apolipoprotein C-III precursor, complement C3 precursor, and [[alpha]. (thefreedictionary.com)
  • Using the models of two long anti-atherogenic and anti-inflammatory proteins (apolipoprotein A-I and apolipoprotein E with 243 and 299 amino acids, respectively) short mimetic peptides of 18 to 28 amino acid residues in length, which can be produced either synthetically or genetically in edible fruits and vegetables, have been shown to exert profound biological effects in a large number of animal models of diseases. (springer.com)
  • Apolipoprotein A-I (apoA-I) is the defining component of all HDLs, which, along with different combinations of proteins, confer many functions to HDLs, the best known being atheroprotection ( 1 ). (rupress.org)
  • Dose-response effects of marine omega-3 fatty acids on apolipoproteins, apolipoprotein-defined lipoprotein subclasses, and Lp-PLA2 in individuals w. (nih.gov)
  • Little evidence exists regarding the dose-response effects of the marine omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on apos, apo-defined Lps, and Lp-PLA2. (nih.gov)
  • Epidemiological studies show that risk of AD varies inversely with consumption of omega-3 fatty acids from fish and seafood. (clinicaltrials.gov)
  • Blood omega-3 fatty acids was evaluated monthly during the supplementation period. (clinicaltrials.gov)
  • In order to test whether hyperlipidaemia and glycaemic control can be improved among diabetes patients by dietary supplementation with purified omega-3 fatty acids, we carried out a double-blind, placebo-controlled trial on 50 type 2 diabetes patients randomized to 2 g/day purified omega-3 fatty acids or placebo for 10 weeks. (who.int)
  • Omega 3 fatty acids induce a marked reduction of apolipoprotein B48 when added to fluvastatin in patients with type 2 diabetes and mixed hyperlipidemia. (greenmedinfo.com)
  • Niacin and omega-3 fatty acids may correct non-HDL lipoprotein and apolipoprotein B abnormalities. (greenmedinfo.com)
  • Three classes of medications are appropriate for the management of major triglyceride elevations: fibric acid derivatives, niacin, and omega-3 fatty acids. (medscape.com)
  • Omega-3 fatty acids are attractive because of their low risk of major adverse effects or interaction with other medications. (medscape.com)
  • Therefore, a minimum dose of 4 g of omega-3 fatty acids per day may require at least 8-12 capsules/day. (medscape.com)
  • Fasting lipid profile was taken when patients were treated with diet, diet plus 80 mg of fluvastatin and diet plus fluvastatin 80 mg and 4 g of prescription omega 3 fatty acids. (biomedcentral.com)
  • Our preliminary findings therefore suggest an additional benefit on postprandial atherogenic particles when omega 3 fatty acids are added to standard treatment with fluvastatin. (biomedcentral.com)
  • We therefore undertook a preliminary evaluation of the effect of the addition of omega 3 fatty acids on the postprandial particles, measured specifically as plasma concentrations of apolipoprotein B48, in diabetic patients with mixed hyperlipidemia receiving treatment with fluvastatin. (biomedcentral.com)
  • We undertook a non-controlled, open-label study of the lipid effects of omega 3 fatty acids when they were added to a low-calorie diet and fluvastatin in patients with type 2 diabetes and mixed hyperlipidemia. (biomedcentral.com)
  • At the third visit, eight weeks after starting the treatment with fluvastatin 80 mg, a further blood sample was taken and, in addition to the diet and the fluvastatin 80 mg, the patients were asked to take 4 capsules of prescription omega 3 fatty acids daily, containing 460 mg of EPA and 380 mg of DHA ethyl esters. (biomedcentral.com)
  • In conclusion lipid and apolipoprotein distributions in Sicilian newborns are not different from that of other population and there are no differences between males and females. (springer.com)
  • G polymorphisms are associated with TG levels in overweight/obese Chinese subjects and that the two polymorphisms are also associated with certain lipid and apolipoprotein variations, depending on BMI. (biomedcentral.com)
  • As assessed in cultured jejunal explants incubated with either [14C]-oleic acid or [35S]-methionine, fish oil feeding resulted in diminished triglyceride-rich lipoprotein assembly and apolipoprotein (apo) B-48 biogenesis, respectively. (ovid.com)
  • Genetic factors contributing to the expression of type III HLP were investigated in 113 hyper- and 52 normolipidemic E2/2 subjects, by testing for polymorphisms in APOC3, APOA5, HL (hepatic lipase) and LPL (lipoprotein lipase) genes. (tudelft.nl)
  • All variants were able to remodel multillamelar 1,2-Dimyristoyl-sn-glycero-3-phosphocholine (DMPC) vesicles, but R136S and R145C had reduced kinetics. (nih.gov)
  • 3. The method of claim 1, wherein the pancreatic β cell specific targeting moiety comprises an antibody or an aptamer. (freepatentsonline.com)
  • There are currently no images for Apolipoprotein M/ApoM Antibody (NB110-60526AF488). (novusbio.com)
  • Ex vivo studies of apoC-III complexes with higher apoC-III2/apoC-III1 showed attenuated inhibition of VLDL uptake by HepG2 cells and LPL-mediated lipolysis, providing possible functional explanations for the inverse association between a higher apoC-III2/apoC-III1 and hypertriglyceridemia, proatherogenic plasma lipid profiles, and cardiovascular risk. (univ-lorraine.fr)
  • Hepatic levels of 3-hydroxy-3-methylglutaryl-CoA reductase mRNA did not vary significantly between the groups. (biochemj.org)
  • The present invention relates to methods of use of phosphonate-phosphates and diphosphonates to modulate apolipoprotein E levels and the use of such compounds in therapy, including cardiovascular and neurological disease states. (freepatentsonline.com)
  • (diabetesjournals.org)
  • In autoimmune disease, anti-apolipoprotein H (AAHA) antibodies, also called anti-β2 glycoprotein I antibodies, comprise a subset of anti-cardiolipin antibodies and lupus anticoagulant. (wikipedia.org)
  • Tantalizingly, a truncated form of apoL-I (Tr-apoL-I) devoid of the SRA-interacting domain, which was expressed in bacteria or conjugated to nanobodies that recognize a common carbohydrate epitope on the variant surface glycoprotein (VSG) coat of trypanosomes, was reported to escape binding of SRA and kill TLF-resistant trypanosomes ( 3 , 8 ). (rupress.org)
  • Since most tilted peptides were shown to induce liposome fusion in vitro, the fusogenic capacity of the 6-20 fragment of apo C-III was tested on unilamellar liposomes and compared with the well characterized SIV fusion peptide. (ucl.ac.uk)
  • Lipid-mixing experiments showed that the apo C-III (6-20) peptide is able to increase the fluorescence of a lipophilic fluorescent probe. (ucl.ac.uk)
  • The apo C-III (6-20) fragment is, however, less fusogenic than the SIV peptide, in agreement with their respective mean hydrophobicity. (ucl.ac.uk)
  • We examined the association between plasma LDL with apoC-III and coronary heart disease in 320 women and 419 men initially free of cardiovascular disease who developed a fatal or nonfatal myocardial infarction during 10 to 14 years of follow-up and matched controls who remained free of coronary heart disease. (harvard.edu)
  • The risk of coronary heart disease contributed by LDL appeared to result to a large extent from LDL that contains apoC-III. (harvard.edu)
  • We investigated whether subspecies of HDL defined by apoC-III are associated with coronary heart disease (CHD). (ovid.com)
  • 3, 4 Furthermore, phenotypes E4/4 and E4/3 have been associated with the risk of myocardial infarction and coronary heart disease,*RF 5-7* particularly in young people, although there is some controversy about this. (bmj.com)
  • Histomorphometry of plaque cross-sectional area in the proximal aortas, en face measurement of plaque area over the aortic trees, Pg 16S ribosomal DNA amplification with polymerase chain reaction, ELISA for systemic proinflammatory mediators, and immunolocalization of macrophages in the proximal aorta were performed. (ahajournals.org)
  • We therefore tested the hypothesis that n-3 fatty acids improve the various events governing intra-enterocyte lipid transport in Psammomys obesus gerbils, a model of nutritionally induced metabolic syndrome. (ovid.com)
  • Rather, the suppressed production of apo B-48 by n-3 fatty acids was associated with intracellular proteasome-mediated posttranslational downregulation in insulin-resistant and diabetic animals. (ovid.com)
  • Epidemiological studies suggest a protective role of omega-3 poly-unsaturated fatty acids (n-3 PUFA) against Alzheimers disease (AD). (eurekaselect.com)
  • Macrophage apolipoprotein-E knockdown modulates caspase-3 activation w" by D A Elliott, Woojin Scott Kim et al. (edu.au)
  • corresponding hazard ratios for apolipoprotein A-I were 1.00 (reference), 0.98 (CI, 0.71 to 1.35), 1.02 (CI, 0.72 to 1.44), 1.37 (CI, 0.98 to 1.90), and 1.58 (CI, 1.14 to 2.20) ( P for linear trend = 0.005). (annals.org)
  • No associations were found for four HL gene polymorphisms and two LPL gene polymorphisms and type III HLP. (tudelft.nl)
  • Polymorphisms in lipolysis genes associate with the expression and severity of type III HLP in APOE2/2. (tudelft.nl)