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Research has been conducted on the membrane lipid hydroperoxides. The hypothesis that these hydroperoxides' translocation from cells to low-density lipoprotein may sensitize the lipoprotein to free radical-mediated oxidative modification has been tested studying spontaneous transfer kinetics of different cholesterol lipid hydroperoxides species via photoperoxidized erythrocyte ghosts as model donors and the details are presented.

Research has been conducted on the initial plasma acceptor of the peripheral cells' unesterified cholesterol and phospholipids. The effect of phospholipids on the pre-beta apoA-I formation during the cholesterol ester transfer protein-mediated remodeling of the high-density lipoproteins has been investigated and the details are reported.

Research has been conducted on the lipid-free apolipoprotein A-I. The structure and stability of the apolipoprotein's central region have been investigated via the study of the effect of mutations on the conformation, size, stability of the high-density lipoprotein particles and the details are reported.

Research has been conducted on the lipovitellin. The molecular structure of this lipoprotein has been investigated and the results indicate that the factors affecting lipoprotein formation can be understood via the study of the lipid and protein interactions.

Results demonstrate that the selective uptake of low-density lipoprotein occurs via different mechanisms as opposed to high-density lipoprotein uptake. The low-density lipoprotein uptake is independent of scavenger receptor SR-BI and is influenced by cell-free cholesterol.

Research has been conducted on the triacylglycerol hydrolase which hydrolizes stored cytoplasmic triaglycerol in liver. The relationship between the structure and activity of this hydrolase have been investigated and the details are reported.

Research has been conducted on clusterin, the extracellular mammalian chaperone binding to the unfolded stressed proteins. The hypothesis that clusterin binds to toxic molecules in the extracellular environment and carries these to the cells expressing lipoprotein receptor-related protein-2 for the uptake and degradation has been tested and the results are reported.

Research has been conducted on the protein 39 kDa receptor-associated protein, a secretory pathway for the low-density lipoprotein receptor family members of the endocytic receptors. The binding of the full-length receptor-associated protein and its isolated domains to the ubiquitin-fused complement-type repeat-domain pairs has been investigated and the results are reported.

Research has been conducted on the complement-like repeat 7. The X-ray structure of the Ca (super)2+ complex of this complement-like repeat 7 from the low-density lipoprotein receptor-related proteins has been investigated and the calcium binding properties have been characterized.

Electron microscopy of lipoprotein(a) reveals that it is a spherical particle without any large projections with the close association of apolipoprotein(a) and apolipoprotein B-100. Conformational analysis shows individual kringle units in each isoform and the number of kringle units correlates with the isoform size of the apolipoprotein(a).

Results show that the minimal structure of a substrate for platelet-activating factor acetylhydrolases (PAF-AHs) is the glyceride derivative that includes an sn-2 ester and an hydrophobic chain. Data indicate that in vivo, the enzymes are bound to high and low density lipoproteins.

Research describes the cloning and characterization of a unique low-density lipoprotein receptor-related protein 9 from mouse lymphocyte cDNA library using an improved signal sequence trap system based on retrovirus-mediated expression screening technique. Results indicate that the new receptor may participate in the uptake of apolipoprotein E containing lipoproteins.

Results demonstrate that chiral N,N-disubstituted trifluro-3-amino-2-propanol compounds inhibit lipid transfer activity of cholesteryl ester transfer protein without affecting its structure. Data show that the chiral center involved in the inhibitory activity consists of two enantiomers, of which one is 10-fold more potent than the other.

Research has been conducted on the mutations within the ligand-binding low-density lipoprotein (LDL) -A modules of the LDL receptor. The impact of two familial hypercholesterolemia mutations in the LDL-A module five and two mutations in module six has been investigated.

Varying stability in the human apolipoprotein (apo) E isoforms determined by the amino-terminal domain are discussed. Study has shown that the major isoforms of apoE show significant differences in stability. Guanidine-HCL denaturation monitored by circular dichroism and fluorescence indicate there is a folding intermediate in apoE, most noticeably in apoE4.

Specificity of lipid incorporation has been determined by sequences in the N-terminal 37% of apolipoprotein B (ApoB). C127 cells were permanently transfected to secrete the N-terminal 29, 32.5 or 37% of apoB. It had been shown already that mouse mammary carcinoma-derived (C127) cells, transfected to express the N-terminal 17% of human apoB (apoB-17), secreted mostly lipid-poor apoB-17 with a peak density less than 1.21 g/ml. the beta-sheets at and beyond apoB-29 are critical for recruiting triacylglycerol (TAG) into nascent lipoprotein.

Serum albumin has been used as a predictor of coronary heart diseases because of its association with cholesterol metabolism and the development of arteriosclerosis. Analysis of the movement of cholesterol into and out of non-cholesterol-loaded fibroblasts has revealed the involvement of albumin in cholesterol transport. Results have shown that albumin operates as a channel which enhances cholesterol transfer between cells and lipoproteins.

The level of the intracellular cholesterol rather than the method of cholesterol release functions as a repressor or activator of the genes that regulate cholesterol in cells. The rate of change in mRNA levels, protein content and the activity of regulatory proteins is the same when rat ovary granulosa cells are cultured with lipoproteins, hLDL or hHDL3. The pretreatment with either of the lipoproteins results in down-regulation of B/E-receptor and HMG CoA reductase proteins and an increase in acyl-CoA:cholesterol acyltransferase activity.

A study of the inhibitory process of Glu-plasminogen binding to fibrin surface reveals that the concentration and affinity of lipoprotein (a) (Lp(a)) towards fibrin and plasminogen mediate in vivo binding of plasminogen or Lp(a) to fibrin. In heterozygous subjects, two Lp(a) motifs help in the inhibition of plasminogen binding. Alterations in equilibrium dissociation constants of Lp(a) particles takes place in plasma of heterozygote individuals containing two isoform phenotype. The results of the measurement of occupancy-dependent dissociation constant are discussed.

The catalytic degradation of lipoproteins by lipoprotein and hepatic lipases was examined to determine the association between phospholipid and triacylglycerol catabolism during lipoprotein remodeling and conversion. The degradation rates of phospholipids and triacylglycerol are highly correlated. Results indicate that removal of triacylglycerol from the core of the lipoprotein is an essentail determinant of phospholipid shedding. Further, removal of phospholipid molecules is an important mechanism in lipoprotein remodelling.

Proton nuclear magnetic resonance of the conformational alteration in the peptide Ac-K-G-R-G-D-G-amide due to a phospholipidic surface to determine the secondary structure arising from the interaction of the peptide and lipids. The peptide is flexible in solution and assumed an unstructured arrangement independent of the presence of micellar structures in solution. On the other hand, when the same peptide was conjugated with a lipid anchor, the lipopeptide assumed a partially ordered conformation in the presence of micellar structures.

The fibroblasts that express either normal LDL receptor (LDLR) or an LDLR variant that is unable to employ the acid-dependent release mechanism were generated to determine the relative contributions of acidic pH and low free calcium on lipoprotein release. The results suggested that endosomes use both the acid-dependent and calcium-dependent release mechanisms to drive lipoprotein release and that the acid-dependent process is only required for LDL release.

Results show that Trans unsaturated fatty acids are protective of lipoprotein oxidation, as shown in artificial membranes, suggesting that they are not involved in atherosclerosis at least with respect to low-density lipoprotein oxidation. Data indicate that dietary trans unsturated fatty acids decrease lipid peroxidation process, thereby reducing the atherogenic effect of them.

Research has been conducted on ATP-binding cassete transporter A1(ABCA1). The authors have investigated the changes in lipoprotein fractions in Abca1-deficient mice, and the mechanisms responsible for HDL low levels in the absence of Abca1.

Research has been conducted on low-density lipoprotein-cholesteryl esters. The hypothesis that receptor class B type I is implicated in low-density lipoprotein-cholesteryl ester selective uptake in human hepatoma cells and mouse hepatic cells has been tested, and the results are described.

Research has been conducted on ST7, a member of low-density lipoprotein superfamily. The authors have investigated the relationship between ST7 and low-density lipoprotein receptor-related superfamily proteins, and they report that ST7 is a member of subfamily of the low-density lipoprotein receptor-related protein superfamily, and that its cytoplasmic domain contains motifs implicated in signal transduction and endocytosis.

Research has been conducted on lipopolysaccharide, a human pathogen Haemophilus influenzae virulence determinant. The study of the lipopolysaccharide structure carried out via the use of electrospray ionization mass spectrometry and high-field NMR techniques on lipopolysaccharide core oligosaccharide samples and on delipidated lipopolysaccharide is described.

Results suggest that naringenin flavonoid inhibits the lipidation and apoB-containing lipoprotein secretion by limiting triglyceride in the endoplasm reticulum lumen by inhibiting the microsomal triglyceride transfer protein activity.