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In vivo morphometry of the intrasulcal gray matter in the human cingulate, paracingulate, and superior-rostral sulci: hemispheric asymmetries, gender differences and probability maps. | Volumes of the intrasulcal gray matter were measured in three cerebral sulci located on the medial wall of the human frontal lobe: cingulate sulcus (CS); paracingulate sulcus (PCS); and superior-rostral sulcus (SRS). The measurements were carried out on T1-weighted 3-D high-resolution magnetic-resonance (MR) images acquired in 105 young right-handed volunteers (42 female and 63 male). Before the measurement; the images were transformed into a standardized stereotaxic space (Talairach and Tournoux [1988] Hum | 8978477 | [
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In vivo morphometry of the intrasulcal gray matter in the human cingulate, paracingulate, and superior-rostral sulci: hemispheric asymmetries, gender differences and probability maps. | an Brain: 3-Dimensional Proportional System. An Approach to Cerebral Imaging. Stuttgart; New York: Georg Thieme Verlag); thus removing inter-individual differences in brain size. The intrasulcal gray matter was segmented in a semi-automatic manner. Significant gender differences were found in the volume of the CS (female > male) and the PCS (male > female). Hemispheric asymmetries were observed between the left and right volumes of the intrasulcal gray matter in the anterior (right > left) and posterior (le | 8978477 | [
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In vivo morphometry of the intrasulcal gray matter in the human cingulate, paracingulate, and superior-rostral sulci: hemispheric asymmetries, gender differences and probability maps. | ft > right) segments of the CS; as well as between the left and right volumes of the PCS (left > right). There was no interaction between the asymmetries and gender. In addition; significant positive correlations were found between the left and right gray-matter volumes in the anterior (r = 0.43) and posterior (r = 0.66) segments of the CS; whereas significant negative correlations were observed between the gray-matter volumes of the anterior segment of the CS and those of the PCS (left hemisphere: r = -0.4 | 8978477 | [
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In vivo morphometry of the intrasulcal gray matter in the human cingulate, paracingulate, and superior-rostral sulci: hemispheric asymmetries, gender differences and probability maps. | 8; right hemisphere: r = -0.42). The observed hemispheric asymmetries in the CS and PCS gray-matter volumes are consistent with the proposed role of these structures in the integration of emotions with cognition (CS) and in the control of speech/vocalization (PCS). The pattern of inter-hemispheric correlations in the sulcal gray-matter points to an increasing asynchrony in the foetal development of primary (CS); secondary (SRS); and tertiary (PCS) sulci; respectively. The presence of negative correlations b | 8978477 | [
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In vivo morphometry of the intrasulcal gray matter in the human cingulate, paracingulate, and superior-rostral sulci: hemispheric asymmetries, gender differences and probability maps. | etween the two neighbouring sulci (CS and PCS) suggests that a process of compensation could underlie interactions between adjacent primary and tertiary sulci. Besides the above volumetric analysis; we also provide average (probability) maps of the three sulci; the use of such maps for the parcellation of the medial frontal lobe and localization of "peaks" obtained in blood-flow activation studies is discussed. | 8978477 | [
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Metabolic fate of oleic acid derived from lysosomal degradation of cholesteryl oleate in human fibroblasts. | Low density lipoprotein cholesteryl [14C]oleate (LDL-[14C]CO) was used as a tool to label lysosomes with cholesteryl [14C]oleate (CO) and to follow subsequently the metabolic processing of oleic acid released by acid lipase. Liberated [14C]oleate was incorporated into glycerolipids; mainly into phosphatidylcholine. Incubations in the presence of various concentrations of exogenously added oleic acid and double label experiments showed that oleic acid derived from lysosomal degradation of CO and exogenously | 8978478 | [
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Metabolic fate of oleic acid derived from lysosomal degradation of cholesteryl oleate in human fibroblasts. | added oleic acid distributed in a similar fashion among triacylglycerol and various phospholipids. To further study the metabolism of LDL-derived oleic acid; experiments were performed in which fibroblasts were prelabeled with LDL-[14C]CO. The subsequent processing of lysosome-derived oleic acid was followed with time without LDL-[14C]CO in the medium. From these experiments it became clear that apart from the esterification into glycerolipids a substantial part of lysosome-derived oleic acid was released i | 8978478 | [
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Metabolic fate of oleic acid derived from lysosomal degradation of cholesteryl oleate in human fibroblasts. | nto the medium. The efflux of oleic acid into the medium preceded the incorporation into glycerolipids; was dependent on the composition of the extracellular medium; and was energy-independent. Our data are compatible with a mechanism in which lysosome-derived fatty acids are transported to the plasma membrane prior to transport to endoplasmic reticulum for esterification. Intra- and extra-cellular factors influence the distribution of lysosome-derived oleic acid among cells and medium. | 8978478 | [
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Cholesta-5,7,9(11)-trien-3 beta-ol found in plasma of patients with Smith-Lemli-Opitz syndrome indicates formation of sterol hydroperoxide. | The Smith-Lemli-Opitz syndrome (SLOS) is an autosomal recessive disorder characterized by accumulation of cholesta-5;7-dien-3 beta-0l caused by a deficiency of the enzyme desaturating this sterol to cholesterol. In addition to other unusual sterols recently found in plasma of patients with SLOS; namely cholesta-5;8-dien-3 beta-ol and 19-nor-cholesta-5;7;9 (10)-trien-3 beta-ol we have detected a trienol and we describe here its identification as cholesta-5;7;9 (11)-trien-3 beta-ol by GC-MS and by comparison | 8978479 | [
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Cholesta-5,7,9(11)-trien-3 beta-ol found in plasma of patients with Smith-Lemli-Opitz syndrome indicates formation of sterol hydroperoxide. | with a synthetic standard. We tested the possibility that the trienol may be formed by radical oxidation of cholesta-5;7-dien-3 beta-ol accumulated in plasma of patients with SLOS because it is known to be formed by decomposition of 7-hydroperoxy-cholesta-5;8-dien-3 beta-ol; which is a product of cholesta-5;7-dien-3 beta-ol photooxidation. Incubation of cholesta-5;7-dien-3 beta-ol with rat liver microsomes in the presence of ADP/Fe2+ and NADPH gave rise to a number of oxygenated sterols. Among these; analys | 8978479 | [
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Cholesta-5,7,9(11)-trien-3 beta-ol found in plasma of patients with Smith-Lemli-Opitz syndrome indicates formation of sterol hydroperoxide. | is by particle-beam LC-MS under CI conditions indicated the presence of 7-hydroperoxy-cholesta-5;8-dien-3 beta-ol and of cholesta-5;7;9(11)-trien-3 beta-ol which is known to derive from the oxidation of the 7-hydroperoxide. From these results we conclude that cholesta-5;7-dien-3 beta-ol accumulated in tissues of patients with SLOS may be oxidized by oxygen radicals giving rise to oxygenated sterols. Some of these compounds may be toxic and may contribute to worsen the pathological picture in patients with S | 8978479 | [
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Cholesta-5,7,9(11)-trien-3 beta-ol found in plasma of patients with Smith-Lemli-Opitz syndrome indicates formation of sterol hydroperoxide. | LOS. | 8978479 | [
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Phytanic acid activation in rat liver peroxisomes is catalyzed by long-chain acyl-CoA synthetase. | In Refsum disease; disorders of peroxisome biogenesis; and rhizomelic chondrodysplasia punctata; pathological accumulation of phytanic acid results from impaired alpha-oxidation of this branched-chain fatty acid. Previous studies from this laboratory indicated that activation of phytanic acid to its CoA derivative precedes its alpha-oxidation in peroxisomes. It was reported that this reaction is catalyzed by a unique phytanoyl-CoA synthetase in human peroxisomes. We wanted to determine whether phytanic acid | 8978480 | [
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Phytanic acid activation in rat liver peroxisomes is catalyzed by long-chain acyl-CoA synthetase. | activation in rats required long-chain acyl-CoA synthetase (LCS); very long-chain acyl-CoA synthetase (VLCS); or a different enzyme. To test directly whether LCS could activate phytanic acid; rat liver cDNA encoding this enzyme was transcribed and translated in vitro. The expressed enzyme had both LCS activity (assayed with palmitic acid; C16: 0) and phytanoyl-CoA synthetase activity; VLCS activity (assayed with lignoceric acid; C24: 0) was not detectable. The ratio of phytanoyl-CoA synthetized activity to | 8978480 | [
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Phytanic acid activation in rat liver peroxisomes is catalyzed by long-chain acyl-CoA synthetase. | palmitoyl-CoA synthetase activity for LCS synthetized in vitro (approximately 205) was higher than that observed in peroxisomes isolated from rat liver (5-10%); suggesting that the expressed enzyme contained sufficient phytanoyl-Coa synthetase activity to account for all activity observed in intact peroxisomes. Further experiments were carried out to verify that phytanic acid was activated by LCS in rat liver peroxisomes. Attempts to separate LCS from phytanoyl-CoA synthetase by chromatography on several m | 8978480 | [
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Phytanic acid activation in rat liver peroxisomes is catalyzed by long-chain acyl-CoA synthetase. | atrices were unsuccessful. Preparative isoelectric focusing revealed that phytanoyl-CoA synthetase and LCS had indistinguishable isoelectric points. Phytanoyl-CoA synthetase activity was inhibited by unlabeled palmitic acid but not by lignoceric acid. Heat treatment inactivated both phytanoyl-CoA and palmitoyl-CoA synthetase activities at similar rates. 5;8;11;14-Eicosatetraynoic acid inhibited activation of phytanic acid and palmitic acid in a parallel dose-dependent manner; whereas activation of lignoceri | 8978480 | [
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Phytanic acid activation in rat liver peroxisomes is catalyzed by long-chain acyl-CoA synthetase. | c acid was not affected. These data support our conclusion that rat liver LCS; an enzyme known to be present in peroxisomal membranes; has phytanoyl-CoA synthetase activity. | 8978480 | [
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Monomethylethanolamine reduces plasma triacylglycerols and apolipoprotein B and increases apolipoprotein A-I rats without induction of fatty liver. | Monomethylethanolamine (MME) inhibits very low density lipoprotein (VLDL) secretion from cultured rat hepatocytes by disruption of translocation of apolipoprotein (apo) B across the endoplasmic reticulum membrane (A. E. Rusiñol; E. Y. W. Chan and J. E. Vance. 1993. J. Biol. Chem. 268: 25168-25175). We have now investigated whether or not plasma levels of lipids and apoB are reduced by dietary supplementation of rats with MME. In rats fed MME for 5 to 7 days; the levels of triacylglycerols and apoB in VLDL w | 8978481 | [
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Monomethylethanolamine reduces plasma triacylglycerols and apolipoprotein B and increases apolipoprotein A-I rats without induction of fatty liver. | ere reduced by 66% and 45%; respectively. At the same time; MME feeding also increased plasma apoA-I by 80%. No significant differences were found in body or liver weights between control and MME-fed rats; nor did the reduction of plasma VLDL in MME-fed rats result in accumulation of triacylglycerols in the liver. When the dietary period was extended to 15 weeks; essentially the same results were obtained except that plasma cholesterol was increased by 31% in MME-treated animals; apparently because of incre | 8978481 | [
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Monomethylethanolamine reduces plasma triacylglycerols and apolipoprotein B and increases apolipoprotein A-I rats without induction of fatty liver. | ased amounts of apoA-I and high density lipoproteins. According to post-mortem and microscopic examination; rats fed MME for 15 weeks were anatomically normal with no indication of any lipid accumulation in the liver. The ability of MME to reduce VLDL secretion and at the same time to increase the level of high density lipoproteins are attractive properties of a therapeutic agent for treatment of atherosclerosis in humans. | 8978481 | [
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Differential scanning calorimetry study of the influence of phospholipid analogs with a carbonyl-terminated sn-2 chain on the interdigitated phases formed by 1-stearoyl-2-capryl-sn-glycero-3-phosphatidylcholine (C18:C10-PC). | Synthetic glycerophosphocholines with highly asymmetric chain lengths form interdigitated bilayers in the gel phase. In nature; phospholipids with one hydrocarbon chain approximately twice as long as the other can arise from the autooxidation of unsaturated linkages in the acyl chain; and thus the oxidation products would contain a carbonyl group at the chain terminus. In this study; we have investigated the thermotropic behavior of bilayers prepared from mixtures of the well-studied; mixed-chain phospholip | 8978482 | [
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Differential scanning calorimetry study of the influence of phospholipid analogs with a carbonyl-terminated sn-2 chain on the interdigitated phases formed by 1-stearoyl-2-capryl-sn-glycero-3-phosphatidylcholine (C18:C10-PC). | id; 1-stearoyl-2-capryl-sn-glycero-3-phosphocholine (C18:C10-PC; 1); with synthetic 1-stearoyl-2-acyl-sn-glycero-3-phosphocholines in which the sn-2 chain is approximately one-half the length of the sn-1 chain and contains a C==O group near the omega terminus. Phase diagrams of binary mixtures of 1 with a chain-terminal ketone-PC analog (2) or with a chain-terminal ester-PC analog (3) in excess water exhibited gel-phase immiscibility over a wide compositional range; but miscibility in the liquid-crystalline | 8978482 | [
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Differential scanning calorimetry study of the influence of phospholipid analogs with a carbonyl-terminated sn-2 chain on the interdigitated phases formed by 1-stearoyl-2-capryl-sn-glycero-3-phosphatidylcholine (C18:C10-PC). | phase. However; 1 was completely miscible with C18:C10:1 delta 10-PC (compound 4); which bears a chain-terminal carbon-carbon double bond; in both the gel and liquid-crystalline phases. The calorimetric data suggest that phosphatidylcholines (PC) with carbonyl-terminated chains; which can be produced by autooxidation of naturally abundant 1-saturated-2-unsaturated phospholipids such as 1-stearoyl-2-oleoyl-PC; may not form the normal triple-chain mixed interdigitated structure characteristic of hydrocarbon- | 8978482 | [
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Differential scanning calorimetry study of the influence of phospholipid analogs with a carbonyl-terminated sn-2 chain on the interdigitated phases formed by 1-stearoyl-2-capryl-sn-glycero-3-phosphatidylcholine (C18:C10-PC). | terminated PCs in gel-phase bilayers. | 8978482 | [
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Dietary linoleic acid increases and palmitic acid decreases hepatic LDL receptor protein and mRNA abundance in young pigs. | The present study was conducted to determine the effects of dietary fatty acids on hepatic LDL receptor (LDLr) protein abundance and mRNA levels. Sixty pigs were randomized into 10 groups and fed corn-soybean meal diets containing three cholesterol levels (0.25%; 0.5%; and 1.0%; w/w) with no added fat; or fats rich (30% of calories) in palmitic acid or linoleic acid. A control group was fed the base diet with no added fat. After 30 days; plasma LDL-cholesterol (LDL-C) levels increased as the dietary cholest | 8978483 | [
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Dietary linoleic acid increases and palmitic acid decreases hepatic LDL receptor protein and mRNA abundance in young pigs. | erol increased (P < 0.05); however; there was no significant effect of either fatty acid. Dietary fatty acids; however; had distinctly different effects on hepatic LDLr protein (analyzed by ELISA) and mRNA (analyzed by Northern blot) abundance. When pigs consumed diets containing 0.25% cholesterol; linoleic acid increased hepatic LDLr protein 40% whereas palmitic acid reduced it 40% (P < 0.05). These changes in LDLr protein abundance were accompanied by parallel changes in hepatic LDLr mRNA; linoleic acid i | 8978483 | [
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Dietary linoleic acid increases and palmitic acid decreases hepatic LDL receptor protein and mRNA abundance in young pigs. | ncreased LDLr mRNA 2-fold (P < 0.01); whereas palmitic acid decreased it 60% (P < 0.01). The differential effects of fatty acids on LDLr expression were only observed at 0.25% cholesterol; suggesting that higher intakes of cholesterol have a dominant and repressive effect on regulation of LDLr expression. Cholesterol intake increased hepatic total cholesterol levels (P < 0.01) while dietary fatty acids had no effect on hepatic sterols. In summary; our results indicate that dietary linoleic acid and palmitic | 8978483 | [
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Dietary linoleic acid increases and palmitic acid decreases hepatic LDL receptor protein and mRNA abundance in young pigs. | acid have markedly different effects on hepatic LDLr protein abundance that are mediated by differential effects on LDLr mRNA and protein levels. Further studies are needed to fully elucidate the molecular mechanisms by which fatty acids regulate LDLr mRNA and protein levels. | 8978483 | [
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Identification of promoter sequences in the 5' untranslated region of the baboon apolipoprotein[a] gene. | Like humans; baboons possess apolipoprotein[a] (apo[a]); a unique protein component of the atherogenic lipoprotein [a] (Lp[a]) particle. Baboon apo[a] also exhibits extensive variation with respect to size and serum levels. In this report; we have cloned the 5' flanking region of the baboon apo[a] gene (I isoform) and performed promoter mapping studies to identify sequences that control apo[a] transcription. The sequence of the baboon apo[a] 5' flanking region is similar to the human gene; and contains two | 8978484 | [
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Identification of promoter sequences in the 5' untranslated region of the baboon apolipoprotein[a] gene. | Alu repeats that distinguish the apo[a] gene from plasminogen and other apo[a]-like genes. The transcription start site for the baboon apo[a]gene is located 85 bp upstream from the major start site for the human apo[a] gene. For promoter mapping studies; we constructed two sets of deletion clones (5' to 3' and 3' to 5') in luciferase reporter plasmids for transfection of hepatic cell lines (HepG2 and HUh7). These experiments showed that the 5' untranslated region (5' UTR) contains a positive promoter elemen | 8978484 | [
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Identification of promoter sequences in the 5' untranslated region of the baboon apolipoprotein[a] gene. | t with 85% identity to the consensus binding site for hepatocyte nuclear factor 1 alpha (HNF-1 alpha); and a negative element that is functional in HepG2 cells; but not Huh7 cells. Transfection assays with HeLa cells showed that the positive promoter element acts in an hepatocyte-specific manner. We also cloned the 5' flanking region from a baboon carrying a null allele that produced no detectable hepatic transcripts or serum isoforms in vivo. Surprisingly; the 5' flanking regions of the null allele possess | 8978484 | [
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Identification of promoter sequences in the 5' untranslated region of the baboon apolipoprotein[a] gene. | ed a promoter that was functional in transfection assays. We conclude that the baboon apo[a] gene 5'UTR contains hepatocyte-specific promoter elements; but that other unknown sequences must influence apo[a] expression in vivo. | 8978484 | [
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Translational regulation of lipoprotein lipase by thyroid hormone is via a cytoplasmic repressor that interacts with the 3' untranslated region. | To better characterize the increase in lipoprotein lipase (LPL) translation by hypothyroidism; adipocytes were prepared from control and hypothyroid rats. Whereas LPL synthesis was higher in hypothyroid adipocytes; with no change in mRNA levels; there was no increase in hormone-sensitive lipase (HSL) synthesis. To determine whether a transacting translation regulatory factor was present; a cytoplasmic fraction was prepared from control and hypothyroid adipocytes; and added to an in vitro translation system | 8978485 | [
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Translational regulation of lipoprotein lipase by thyroid hormone is via a cytoplasmic repressor that interacts with the 3' untranslated region. | containing the hLPL mRNA. The hypothyroid cell fraction from adipose and heart yielded an increase in LPL translation; when compared to control extracts. Further experiments determined that the control adipocyte extract contained a translation-inhibitory factor that was 8-fold lower in activity in the hypothyroid extract. Using different LPL mRNA constructs in the in vitro translation reaction; the region that controlled translation was localized to nucleotides 1599 to 1638 (proximal 3' untranslated region | 8978485 | [
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Translational regulation of lipoprotein lipase by thyroid hormone is via a cytoplasmic repressor that interacts with the 3' untranslated region. | (UTR)). To confirm the presence of a transacting factor; a sense RNA strand corresponding to this region was added to the in vitro translation reaction. This sense strand competed for the transacting factor in the control cell extract; yet had no effect on the hypothyroid cell extract. Thus; there is a translation repressor factor in the cytoplasm of rat adipocytes; and this factor is greatly reduced in activity in hypothyroid rat adipocytes. Because a similar mechanism of LPL regulation occurs in response | 8978485 | [
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Translational regulation of lipoprotein lipase by thyroid hormone is via a cytoplasmic repressor that interacts with the 3' untranslated region. | to epinephrine; the absence of the translation repressor may be a mechanism for the loss of sensitivity of hypothyroid cells for catecholamines. | 8978485 | [
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Characterization of the murine phosphatidylethanolamine N-methyltransferase-2 gene. | Phosphatidylethanolamine N-methyltransferase (PEMT) catalyzes the conversion of phosphatidylethanolamine to phosphatidylcholine in the mammalian liver via three sequential methylations. In the present studies; we cloned and characterized the murine gene for PEMT2; the isoform of the enzyme that localized to the mitochondria-associated membrane. The structure of the gene was determined by analysis of two lambda and three P1 genomic clones; and compared to the known rat PEMT2 cDNA sequence. Southern blotting | 8978486 | [
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Characterization of the murine phosphatidylethanolamine N-methyltransferase-2 gene. | of mouse genomic DNA indicated that PEMT2 is a single-copy gene. The gene spans at least 35 kb; with seven exons and six introns. Two transcription start sites; 139 and 148 base pairs upstream of the translation start site; were detected by primer extension and reverse transcriptase-polymerase chain reaction. These experiments indicated that the PEMT2 gene is transcribed from a single promoter. Finally; the PEMT2 gene was localized to mouse chromosome 11 by interspecific backcrossing. These experiments repr | 8978486 | [
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Characterization of the murine phosphatidylethanolamine N-methyltransferase-2 gene. | esent the first cloning and characterization of a full-length mammalian gene involved in phospholipid biosynthesis. | 8978486 | [
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Metabolism of hydroperoxy-phospholipids in human hepatoma HepG2 cells. | Two enzymatic mechanisms have been proposed for the metabolism of hydroperoxy-phospholipids: i) the combined action of phospholipase A2 and glutathione peroxidase; and/or ii) direct enzymatic reduction. The latter reaction may be catalyzed by selenium-dependent phospholipid hydroperoxide glutathione peroxidase and/or by glutathione S-transferase alpha. To study the pathway of this reaction; we used human hepatoma HepG2 cells into which was incorporated labeled; hydroperoxy-phospholipids. The major product o | 8978487 | [
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Metabolism of hydroperoxy-phospholipids in human hepatoma HepG2 cells. | f incorporated l-palmitoyl-2-(13-hydroperoxy-cis-9; trans-11-octadecadienoyl)-L-3-phosphatidylcholine was the corresponding hydroxy-phospholipid with no hydroxy- or hydroperoxy-fatty acids. The contributions to reduction of hydroperoxy-phospholipids in HepG2 cells from glutathione S-transferase Al and phospholipid hydroperoxide glutathione peroxidase were calculated to be 0.5% and 99.5%; respectively. Increasing selenium in the cell culture medium led to increases in selenium-dependent phospholipid hydroper | 8978487 | [
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Metabolism of hydroperoxy-phospholipids in human hepatoma HepG2 cells. | oxide glutathione peroxidase activity but not in glutathione S-transferase alpha. This increase in the selenium-dependent enzyme was paralleled by a concomitant increase in the extent of reduction of the incorporated hydroperoxy-phospholipid. We conclude that the main metabolic fate of hydroperoxy-phospholipids in HepG2 cells is by direct reduction to hydroxy-phospholipids by phospholipid hydroperoxide glutathione peroxidase but also by glutathione S-transferase alpha; and that phospholipase A2/selenium-dep | 8978487 | [
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Metabolism of hydroperoxy-phospholipids in human hepatoma HepG2 cells. | endent glutathione peroxidase does not play a significant role in the reduction. | 8978487 | [
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Hypocholesterolemic actions of atorvastatin are associated with alterations on hepatic cholesterol metabolism and lipoprotein composition in the guinea pig. | Guinea pigs were fed 15% (w/W) fat; high in lauric and myristic acids; a diet known to produce hypercholesterolemia in these animals. The diet was given alone or in combination with four doses of atorvastatin equivalent to 1; 3; 10; and 20 mg/kg per day. Atorvastatin reduced plasma LDL cholesterol concentrations by 46; 50; 53; and 70%; respectively (P < 0.001). Plasma apoB concentrations were reduced by atorvastatin (P < 0.001) and compositional changes occurred in VLDL and LDL with reductions of the relati | 8978489 | [
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Hypocholesterolemic actions of atorvastatin are associated with alterations on hepatic cholesterol metabolism and lipoprotein composition in the guinea pig. | ve proportion of cholesteryl ester and increases in triacylglycerol. A reduction in hepatic cholesteryl ester (66%) was observed only with the highest atorvastatin dose (20 mg/kg per day) while microsomal cholesterol was reduced by 30% with 3-20 mg/kg per day. Hepatic ACAT activity was down-regulated and apoB/E receptor number was increased by atorvastatin. In contrast; HMG-CoA reductase activity and cholesterol 7 alpha-hydroxylase were not affected by the drug. VLDL apoB secretion rates were decreased by a | 8978489 | [
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Hypocholesterolemic actions of atorvastatin are associated with alterations on hepatic cholesterol metabolism and lipoprotein composition in the guinea pig. | torvastatin treatment 59 and 76% with 3 and 20 mg/kg per day; respectively. Nascent VLDL particles were larger after drug treatment; showing an increased number in triacylglycerol molecules. These results support the hypothesis that the plasma LDL lowering induced by atorvastatin is due to a decreased secretion of apoB in combination with an increase of hepatic apoB/E receptors. | 8978489 | [
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] |
Effects of weekly LDL-apheresis on metabolic parameters of apolipoprotein B in heterozygous familial hypercholesterolemia. | Apheresis is a treatment option for patients with severe hypercholesterolemia and coronary artery disease. It is; however; unknown whether such therapy changes kinetic parameters of lipoprotein metabolism; such as apolipoprotein B (apoB) secretion rates; conversion rates; and fractional catabolic rates (FCR). We studied the long-term effect of regular apheresis therapy on metabolic parameters of apoB in five patients with heterozygous familial hypercholesterolemia (FH) using endogenous labeling with D3-leuc | 8978490 | [
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Effects of weekly LDL-apheresis on metabolic parameters of apolipoprotein B in heterozygous familial hypercholesterolemia. | ine; mass spectrometry; and multicompartmental modeling. Patients were studied prior to (study 1) and after 3-6 months of weekly apheresis therapy (study 2). LDL-apoB concentration was 183 +/- 16 mg d-1 prior to apheresis therapy (study 1); 135 %/- 7 mg. dl-1 at the beginning of study 2; and 163 +/- 10 mg . dl-1 at the end of study 2. VLDL-apoB and IDL-apoB were not different between the two studies and did not change during study 2. Separate modeling of the two studies revealed very similar parameters in e | 8978490 | [
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Effects of weekly LDL-apheresis on metabolic parameters of apolipoprotein B in heterozygous familial hypercholesterolemia. | ach patient. In a second step simultaneous modeling of both studies was performed taking the changing pool size as a non-steady-state condition into account. ApoB tracer data of both kinetic studies and the change in pool size could be described with one set of kinetic parameters (VLDL-apoB FCR 4.32 +/- 1.06 d-1; LDL-apoB FCR 0.17 +/- 0.05 d-1; apoB secretion rate 11.9 +/- 3.7 mg . kg-1 . d-1). These parameters are well within the range of those previously published for FH heterozygotes in steady state. We | 8978490 | [
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Effects of weekly LDL-apheresis on metabolic parameters of apolipoprotein B in heterozygous familial hypercholesterolemia. | conclude that regular apheresis therapy did not alter kinetic parameters of apoB metabolism in these patients with heterozygous FH in the long term and that the decreased rate of delivery of neutral lipids or apoB to the liver does not regulate plasma apoB metabolism. | 8978490 | [
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Formation of oxysterols during oxidation of low density lipoprotein by peroxynitrite, myoglobin, and copper. | Oxidation of low density lipoprotein (LDL) in the artery wall leads to the formation of cholesterol oxidation products that may result in cytotoxicity. Different mechanisms could contribute to LDL oxidation in vivo resulting in characteristic and specific modification of the cholesterol molecule. Alternatively; attack on cholesterol by chain propagating peroxyl radicals could result in the same distribution of oxidation products irrespective of the initial pro-oxidant mechanism. To distinguish between these | 8978488 | [
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Formation of oxysterols during oxidation of low density lipoprotein by peroxynitrite, myoglobin, and copper. | possibilities we have monitored the formation of nine oxysterols during LDL oxidation; promoted by copper; myoglobin; peroxynitrite; or azo bis amidino propane. Regardless of the oxidant used; the pattern of oxysterol formation was essentially the same. The yields of products identified decreased in the order 7-oxocholesterol > 7 beta-hydroxycholesterol > 7 alpha-hydroxycholesterol > 5;6 beta-epoxycholesterol > 5;6 alpha-epoxycholesterol except in the case of peroxynitrite in which case a higher yield of 5 | 8978488 | [
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Formation of oxysterols during oxidation of low density lipoprotein by peroxynitrite, myoglobin, and copper. | ; 6 beta-epoxycholesterol relative to 7-oxocholesterol was found. No formation of cholestane 3 beta; 5 alpha; 6 beta-triol; or the 24-;25-;27-hydroxycholesterols was seen. Concentration of 7-oxocholesterol levels in LDL was positively correlated with the degree of protein modification. Endogenous alpha-tocopherol in LDL or supplementation with butylated hydroxytoluene prevented oxysterol formation. Taken together these data indicate that the oxidation of cholesterol and protein in LDL occur as secondary oxi | 8978488 | [
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Dimeric lipoprotein lipase is bound to triglyceride-rich plasma lipoproteins. | Lipoprotein lipase hydrolyzes the triglyceride-rich core of chylomicrons and very low density lipoproteins. It is also a ligand; in vitro; for binding of lipoproteins to the low density lipoprotein receptor-related protein and may play a central role in the receptor-mediated removal of triglyceride-rich lipoproteins. The aim of the present study was to determine to which lipoprotein subclass the enzyme is bound in preheparin plasma and when released into plasma by heparin injection. Tetrahydrolipstatin; a p | 8978491 | [
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Dimeric lipoprotein lipase is bound to triglyceride-rich plasma lipoproteins. | otent inhibitor of serine lipases; was used to block lipolytic activity; thereby preventing changes in plasma lipoproteins due to ex vivo lipolysis. To analyze the distribution pattern of lipoprotein lipase dimers among lipoprotein classes; a specific ELISA was used and gel filtration was performed in pre- and postheparin plasma from five subjects with triglyceride ranging from 69 to 522 mg/dl. When lipolytic activity was not inhibited; lipoprotein lipase dimers eluted in association with low and high densi | 8978491 | [
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Dimeric lipoprotein lipase is bound to triglyceride-rich plasma lipoproteins. | ty lipoproteins; reproducing results previously obtained by several groups of investigators. However; in pre- and postheparin samples treated with tetrahydrolipstatin; most of the dimeric enzyme was found associated with very low density lipoprotein particles. In conclusion in pre- and postheparin samples most of the lipoprotein lipase dimers are associated with very low density lipoproteins when ex vivo lipolytic activity is inhibited; which supports the hypothesis that; in vivo; lipoprotein lipase may aff | 8978491 | [
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Dimeric lipoprotein lipase is bound to triglyceride-rich plasma lipoproteins. | ect the receptor-mediated removal of these particles. Moreover; it suggests that the association between lipoprotein lipase and cholesterol-rich lipoproteins might be an ex vivo phenomenon due to lack of inhibition of lipolytic activity. | 8978491 | [
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A comparative study of sterol absorption in different small-intestinal brush border membrane models. | We reported previously that the absorption of cholesterol and long-chain cholesteryl esters by rabbit small-intestinal brush border membranes (BBMV) is protein-mediated (Thurnhofer; H.; and H. Hauser. 1990. Biochemistry. 29:2142-2148; Compassi; S.; M. Werder; D. Boffelli; F. E. Weber; H. Hauser; and G. Schulthess. 1995. Biochemistry. 34: 16473-16482). Evidence is presented for similar cholesterol transport activities in rabbit; pig; and human BBMV. As BBMV are subject to a number of limitations and the infl | 8978492 | [
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A comparative study of sterol absorption in different small-intestinal brush border membrane models. | uence of these on sterol absorption is unknown; it is desirable to verify results obtained with this model system in other brush border membrane models more closely related to the in vivo situation. Sterol absorption in intact enterocytes parallels the absorption measured in BBMV; provided that both model systems are normalized to equal sucrase activity. The parallel behavior of the two brush border membrane models lends support to our previous conclusion that the brush border membrane takes up free and est | 8978492 | [
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A comparative study of sterol absorption in different small-intestinal brush border membrane models. | erified cholesterol in a facilitated and energy-independent process. The absorption of sterols in small-intestinal segments mounted in the Ussing chamber is shown to be a complex process in which the diffusion of the bile salt micelles to the brush border membrane is rate-limiting. All brush border membrane models share the disadvantage of being unstable and subject to degradation. The seriousness of the problem increases apparently with the complexity of the model; i.e.; in the order BBMV-->enterocytes-->i | 8978492 | [
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A comparative study of sterol absorption in different small-intestinal brush border membrane models. | ntestinal segments. One main conclusion of this study is that no brush border membrane model is sufficient and satisfactory; therefore conclusive work in lipid absorption can never be based on a single brush border membrane model. | 8978492 | [
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Aberrantly spliced mRNAs of the 3-hydroxy-3-methylglutaryl coenzyme A lyase (HL) gene with a donor splice-site point mutation produce hereditary HL deficiency. | A novel point mutation in the 3-hydroxy-3methyl-glutaryl coenzyme A lyase gene was found in a Turkish patient with homozygous 3-hydroxy-3-methylglutaric acidemia. Amplification by RT-PCR of the mRNA using a six different pairs of oligonucleotides produced no differences in four of the fragments amplified with respect to the control; but generated two fragments of different size. One was representative of a deletion of 126 bp and the other of an insertion of 78 bp. These abnormal mRNAs resulted from a G-->C | 8978493 | [
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Aberrantly spliced mRNAs of the 3-hydroxy-3-methylglutaryl coenzyme A lyase (HL) gene with a donor splice-site point mutation produce hereditary HL deficiency. | transversion at the nucleotide +1 of an intron; which changed the invariant GT dinucleotide of the 5' donor splice site. This was associated with the occurrence of an alternative splicing; which led to the skipping of the whole exon of 126 bp; and also with the activation of one cryptic donor splice site in the same intron. These aberrant spliced mRNAs are predicted to encode two abnormal HMG-CoA lyase proteins: the first results in a protein with an internal deletion of 42 amino acids; whose enzyme activit | 8978493 | [
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Aberrantly spliced mRNAs of the 3-hydroxy-3-methylglutaryl coenzyme A lyase (HL) gene with a donor splice-site point mutation produce hereditary HL deficiency. | y is largely abolished; as the catalytic site was completely removed; the second contains 17 missense amino acids that precede a stop codon. Northern blot analysis showed that the overall content of these aberrantly spliced mRNAs in proband fibroblasts was the same as that found in control fibroblasts. However; hardly any transcript was observed corresponding to the inserted mutated mRNA when it was examined by a specific probe. To quantify the relative proportion of the two mRNAs; a quantitative RT-PCR (th | 8978493 | [
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Aberrantly spliced mRNAs of the 3-hydroxy-3-methylglutaryl coenzyme A lyase (HL) gene with a donor splice-site point mutation produce hereditary HL deficiency. | e DNA-mimic PCR reaction) was carried out. Results show that the proportion of the inserted mRNAs with respect to the deleted mRNA is only 1.2%. The father; mother; and two brothers of the proband were heterozygous in the G-->C mutation in the +1 nucleotide of the intron considered; while the two alleles of another brother were free of the mutation. | 8978493 | [
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Measurement of 3 beta-hydroxysteroid delta 7-reductase activity in cultured skin fibroblasts utilizing ergosterol as a substrate: a new method for the diagnosis of the Smith-Lemli-Opitz syndrome. | A new sensitive and specific method for the evaluation of 3 beta-hydroxysteroid delta 7-reductase activity; the defective enzyme in the Smith-Lemli-Opitz (SLO) syndrome; is described. The assay is based on the use of gas chromatography-mass spectrometry with selected-ion monitoring to measure the mass of brassicasterol (ergosta-5;22-dien-3 beta-ol) produced by the incubation of ergosterol (ergosta-5;7;22-trien-3 beta-ol) with cultured human skin fibroblasts. Although the conversion of ergosterol to brassica | 8978494 | [
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Measurement of 3 beta-hydroxysteroid delta 7-reductase activity in cultured skin fibroblasts utilizing ergosterol as a substrate: a new method for the diagnosis of the Smith-Lemli-Opitz syndrome. | sterol was slower than the transformation of [3H]7-dehydrocholesterol to [3H] cholesterol; cells from control subjects produced brassicasterol efficiently. In contrast; cells form SLO patients produced very little brassicasterol (P < 0.0001; patients vs. parents or vs. controls). These results indicate that the reduction of ergosterol can be used as an assay for 3 beta-hydroxysteroid delta 7-reductase in human skin fibroblasts; which avoids the many problems caused by the instability and lack of availabilit | 8978494 | [
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Measurement of 3 beta-hydroxysteroid delta 7-reductase activity in cultured skin fibroblasts utilizing ergosterol as a substrate: a new method for the diagnosis of the Smith-Lemli-Opitz syndrome. | y of radiolabeled 7-dehydrocholesterol. The present method made it possible to diagnose the SLO syndrome with high sensitivity and reliability using a commercially available compound. | 8978494 | [
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Lipoprotein lipase degradation by adipocytes: receptor-associated protein (RAP)-sensitive and proteoglycan-mediated pathways. | Lipoprotein lipase (LPL); the major enzyme responsible for the hydrolysis of triglycerides; is primarily synthesized by adipocytes and myocytes. In addition to synthesis; degradation of cell surface-associated LPL is thought to be important in regulating production of the enzyme. We studied LPL metabolism in the LPL synthesizing adipocyte cell line BFC-1 beta and assessed the contributions of cell surface heparan sulfate proteoglycans (HSPG); low density lipoprotein receptor related protein (LRP); and glyco | 8978495 | [
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Lipoprotein lipase degradation by adipocytes: receptor-associated protein (RAP)-sensitive and proteoglycan-mediated pathways. | sylphosphatidylinositol (GPI)-linked proteins to LPL uptake and degradation by these cells. Adipocytes degraded 10-12% of total cell surface I-labeled LPL in 2 h and 23-28% in 4 h. In 1 h; 30-54% of the degradation was inhibited by the 39 kDa receptor associated protein (RAP); an inhibitor of ligand binding to LRP. At 4 h; only 19-23% of the LPL degradation was RAP inhibitable. This suggested that two pathways with different kinetics were important for LPL degradation. Heparinase/heparitinase treatment of c | 8978495 | [
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Lipoprotein lipase degradation by adipocytes: receptor-associated protein (RAP)-sensitive and proteoglycan-mediated pathways. | ells showed that most LPL degradation required the presence of HSPG. Treatment with phosphatidylinositol-specific phospholipase C (PIPLC) inhibited 125I-labeled LPL degradation by 13%. However; neither RAP nor PIPLC treatment of adipocytes significantly increased the amount of endogenously produced LPL activity in the media. To determine whether direct uptake of LPL bound to HSPG could account for the non-RAP sensitive LPL uptake and degradation; proteoglycan metabolism was assessed by labeling cells with 3 | 8978495 | [
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Lipoprotein lipase degradation by adipocytes: receptor-associated protein (RAP)-sensitive and proteoglycan-mediated pathways. | 5SO4. Of the total pericellular proteoglycans; 14% were PIPLC releasable; surprisingly; 30% were dissociated from the cells with heparin. The amount of labeled pericellular proteoglycans decreased 26% in 2 h and 50% in 8 h; rapid enough to account for at least half of the degradation of cell surface LPL. We conclude that adipocytes degrade a fraction of the cell surface LPL; and that this process is mediated by both proteoglycans and RAP-sensitive receptors. | 8978495 | [
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Quantitation of individual phospholipid molecular species by UV absorption measurements. | To validate the utility of on-line measurements of UV absorption for the direct quantitation of individual phospholipid molecular species isolated by reverse-phase HPLC; we synthesized 37 different individual molecular species of diacyl choline glycerophospholipids. UV absorbance response factors (integrate UV absorbance/nmole phospholipid) were calculated for all diacyl; alkenylacyl; and alkylacyl species by injecting varying amounts of the purified molecular species in the 2-100 nmole range and integratin | 8978496 | [
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] |
Quantitation of individual phospholipid molecular species by UV absorption measurements. | g the UV absorbance at 203 nm. There was excellent agreement between the results of the quantitation of individual molecular species determined by measurements of phospholipid mass in HPLC fractions with that based on measurements of total integrated UV absorption and the use of absorbance response factors. The on-line quantitation of individual phospholipid molecular species by UV absorption measurement should prove useful as an adjunct to other techniques of phospholipid quantitation; as a means to assist | 8978496 | [
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Quantitation of individual phospholipid molecular species by UV absorption measurements. | in the identification of individual molecular species in complex biologic mixtures; and as a stand-alone approach to phospholipid quantitation to facilitate studies of the metabolism of individual species particularly when coupled with radiolabeling techniques. | 8978496 | [
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Measurement of small high density lipoprotein subclass by an improved immunoblotting technique. | An improved method of immunoblotting of plasma onto agarose gel matrix containing antiapolipoprotein A-I is described. Fresh plasma samples were subjected to gradient polyacrylamide gel electrophoresis (4-25%) followed by electrotransfer onto agarose gel layer containing antiapolipoprotein A-I. This method was compared with immunoblotting onto nitrocellulose where the transfer onto agarose gel matrix has been shown to be more convenient; quantitative; and can be kept permanently. Plasma apolipoprotein A-I w | 8978497 | [
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Measurement of small high density lipoprotein subclass by an improved immunoblotting technique. | as found to be distributed among regions of varying molecular weights ranging from 43;000 to 800;000. A small size fraction of molecular weight range of 43;000-50;000 (small HDL) was found in normolipidemic and hyperlipidemic subjects. The proportion of the latter fraction varied considerably among subjects (range: 0.0-32%); being lower in normolipidemic subjects (mean +/- SEM: 11.6 +/- 1.4%); and higher in hyperlipidemic subjects (mean +/- SEM: 23.7 %/- 1.7%; P < 0.001). Physiological increase in the level | 8978497 | [
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Measurement of small high density lipoprotein subclass by an improved immunoblotting technique. | of the small HDL was observed in normolipidemic subjects 4 h after fat ingestion (difference: 5.0%; P < 0.001); moreover; the level was higher in normolipidemic subjects who consumed moderate amounts of alcohol (mean +/- SEM: 17.9 +/- 1.2%; P < 0.001) compared with normolipidemic subjects who do not drink alcohol at all. | 8978497 | [
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Signaling effects of alpha-thrombin and SFLLRN in rat glioma C6 cells. | Effects of thrombin on brain cells; including change of neurite outgrowth and astrocyte shape; are described; but the molecular mechanisms are unclear. We investigated the effects of human alpha-thrombin and a six amino acid thrombin receptor activating peptide (TRAP-6; SFLLRN) on [Ca2+]i; phosphoinositide hydrolysis; and protein kinase C in rat glioma C6 cells. Stimulation of C6 cells with both alpha-thrombin and TRAP-6 resulted in [Ca2+]i mobilization; [3H]Inositol phosphate response; and enhanced immunor | 8978498 | [
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Signaling effects of alpha-thrombin and SFLLRN in rat glioma C6 cells. | eactivity of the protein kinase C (PKC) isoenzymes alpha; beta; gamma; delta; and epsilon. Results suggest that alpha-thrombin and TRAP-6 activate at least partially the same intracellular signaling pathways in rat glioma C6 cells; which is evidence for involvement of "tethered ligand" receptor in thrombin induced signaling in glioma C6 cells. | 8978498 | [
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Intracellular localization of heat shock mRNAs (hsc70 and hsp70) to neural cell bodies and processes in the control and hyperthermic rabbit brain. | Heat shock proteins are essential cellular proteins that may play important roles in cellular repair and/or protection. This report focuses on the expression of two members of the hsp70 multigene family; namely; constitutive hsc70 mRNA and stress-inducible hsp70 mRNA in the control and hyperthermic rabbit brain. The intracellular localization of these heat shock mRNAs was examined using high-resolution nonradioactive in situ hybridization. The distribution of hsc70 mRNA and hsp70 mRNA was examined in (1) ne | 8978499 | [
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Intracellular localization of heat shock mRNAs (hsc70 and hsp70) to neural cell bodies and processes in the control and hyperthermic rabbit brain. | uronal cell bodies and their dendritic processes and (2) oligodendrocytes and their cellular processes. In control animals; hsc70 mRNA was detected in the apical dendritic processes and cell bodies of cortical layer II and V neurons; CA3 and CA4 neurons; deep cerebellar neurons; and brainstem neurons. A time course analysis of hsc70 mRNA; after a physiologically relevant increase in body temperature of 2.6 degrees C; revealed more distal transport of this constitutive message into dendrites of these neurona | 8978499 | [
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Intracellular localization of heat shock mRNAs (hsc70 and hsp70) to neural cell bodies and processes in the control and hyperthermic rabbit brain. | l populations. In the same neuronal populations; basal levels of hsp70 mRNA were observed in the cell body; however; this mRNA was not detected in dendritic processes in control or hyperthermic animals. After hyperthermia; hsp70 mRNA was strongly induced in oligodendrocytes and transported to the processes of these glial cells. The localization of heat shock messages in the processes of these neural cell types could provide a mechanism for local control of synthesis of heat shock proteins in cellular compar | 8978499 | [
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Intracellular localization of heat shock mRNAs (hsc70 and hsp70) to neural cell bodies and processes in the control and hyperthermic rabbit brain. | tments that are remote from the cell body. | 8978499 | [
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Genetic elevation of monoamine oxidase levels in dopaminergic PC12 cells results in increased free radical damage and sensitivity to MPTP. | Production of hydrogen peroxide as a by-product of the breakdown of catecholamines by the enzyme monoamine oxidase (MAO) has been hypothesized to contribute to the increased proclivity of dopaminergic neurons for oxidative injury. We established clonal dopaminergic PC12 cell lines which have elevated MAO activity levels resulting from transgenic expression of the B isoform of the enzyme. Both MAO-A and MAO-B have relatively equivalent affinities for dopamine; and since PC12 primarily express the A and not t | 8978500 | [
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Genetic elevation of monoamine oxidase levels in dopaminergic PC12 cells results in increased free radical damage and sensitivity to MPTP. | he B form of the enzyme; this allowed us to distinguish the transgenic MAO activity in these cells from endogenous using the MAO-B specific substrate PEA. Elevation of MAO activity levels in the MAO-B+ cells resulted in higher levels of both free radicals and free radical damage compared with controls. In addition; increased MAO-B levels within PC12 cells caused a dose-dependent increase in sensitivity to the toxin MPTP. Our data suggests that oxidation of catecholamines by MAO can contribute to free radica | 8978500 | [
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Genetic elevation of monoamine oxidase levels in dopaminergic PC12 cells results in increased free radical damage and sensitivity to MPTP. | l damage in catecholaminergic neurons and that the low MAO-B activity levels found endogenously in these cells likely accounts for their relative resistance to MPTP toxicity. | 8978500 | [
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Ex vivo astroglial-induced radial glia express in vivo markers. | Ex vivo induction of radial-like glia has been previously reported to occur following exposure of cerebral cortex subcultures from fetal origin to cerebral cortex astroglial-conditioned medium. The present report further confirms similarities between in vivo and ex vivo radial glia; using additional criteria: adhesion of primary cell dissociates to glial processes; with presumptive cell migration along them; punctuate labelling for laminin; and immunolabelling with Rat-401 antisera. | 8978501 | [
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Distinct mechanisms of neurotransmitter release from PC 12 cells exposed to lead. | Two enzymes; protein kinase C and microsomal Ca(2+)-ATPase help regulate levels of Ca2+ in many types of cells. Since proteins that regulate Ca2+ often influence sensitivity to Pb2+; we determined the possible roles played by protein kinase C and microsomal Ca(2+)-ATPase for the Pb(2+)-evoked release of norepinephrine (NOR) in PC cells. NOR release was observed at 10 microM Pb2+ when PC 12 cells were stimulated with inhibitors of microsomal Ca(2+)-ATPase such as thapsigargin; cyclopiazonic acid; or 2;5-di-( | 8978502 | [
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Distinct mechanisms of neurotransmitter release from PC 12 cells exposed to lead. | t-butyl)-hydroquinone. At 5 microM; Pb2+ evoked the release of NOR in PC 12 cells stimulated with activators of protein kinase C such as phorbol 12-myristate 13-acetate (PMA) or (-)-7-octylindolactam. NOR release was observed at 1 microM Pb2+ in the presence of both PMA and thapsigargin. Ni2+ and Cd2+ blocked NOR release stimulated by Pb2+ in the presence of thapsigargin but not by PMA. NOR released by thapsigargin stimulation was not altered in PC 12 cells depleted of protein kinase C. Two proteins found i | 8978502 | [
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Distinct mechanisms of neurotransmitter release from PC 12 cells exposed to lead. | n vesicles; chromogranin B and secretogranin-II were released with NOR. Our results indicate that in PC 12 cells; PB(2+)-evokes the release of neurotransmitters. Furthermore; thapsigargin and PMA increase the cell's sensitivity to Pb2+ by different pathways. | 8978502 | [
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Ultrastructural localization of 5-hydroxytryptamine1A receptors in the rat brain. | 5-Hydroxytryptamine1A (5-HT1A) receptors have been visualized at the electron microscopic level in selected areas (dorsal raphe nucleus; hippocampus; septum) of the rat brain using specific anti-peptide antibodies. 5-HT1A receptor immunoreactivity was found almost exclusively in the somatodendritic compartment of neurons and was very rarely observed within processes possibly belonging to glial cells. The immunoenzymatic reaction product was associated exclusively with dendritic spines in the dorsal hippocam | 8978504 | [
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Ultrastructural localization of 5-hydroxytryptamine1A receptors in the rat brain. | pus; whereas in the dorsal raphe nucleus and the septal complex; immunoreactivity was found in both dendritic processes and somata. Although some immunolabeling was observed within the cytoplasm of cell bodies; 5-HT1A receptor immunoreactivity was essentially confined to the plasma membrane where it was unevenly distributed. It was frequently associated with synapses (except in the dorsal raphe nucleus); but was also found extrasynaptically in both somata and dendrites. These data suggest that the action of | 8978504 | [
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Ultrastructural localization of 5-hydroxytryptamine1A receptors in the rat brain. | serotonin via 5-HT1A receptor could occur through junctional as well as nonjunctional transmission. | 8978504 | [
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Generation of a monoclonal antibody to the carboxy-terminal domain of tau by immunization with the amino-terminal domain of the amyloid precursor protein. | A fusion protein between beta-galactosidase and the amino-terminal domain of amyloid precursor protein (APP) was used as an immunogen for the production of monoclonal antibodies. One of these antibodies; the 5D12 monoclonal antibody; labeled the neurofibrillary tangles (NFT) by immunohistochemistry; as well as isolated paired helical filaments (PHF) in electron microscopy. In immunoassay; the ascitic fluid produced by the 5D12 clone was demonstrated to contain a high titer of antibodies to heat-stable micro | 8978505 | [
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Generation of a monoclonal antibody to the carboxy-terminal domain of tau by immunization with the amino-terminal domain of the amyloid precursor protein. | tubule associated proteins (MAPs). By immunoblotting; the proteins recognized in heat-stable MAPs were found to correspond to tau proteins. The 5D12 antibody recognized normal tau isolated from rat and human brain homogenates; and PHF-tau isolated from the brain of patients with Alzheimer's disease (AD). By immunoblotting; the 5D12 antibody also recognized the full-length recombinant tau protein but not the fusion protein used as an immunogen. The immunoreactivity of the 5D12 antibody with tau was completel | 8978505 | [
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Generation of a monoclonal antibody to the carboxy-terminal domain of tau by immunization with the amino-terminal domain of the amyloid precursor protein. | y abolished when the half-carboxy domain of tau; containing the tubulin-binding repeats; was removed. This study demonstrates that the use of the amino-terminal domain of APP as an immunogen led to the generation of a monoclonal antibody to the half-carboxy domain of tau. | 8978505 | [
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Nerve growth factor-stimulated mitogen-activated protein kinase activity is not necessary for neurite outgrowth of chick dorsal root ganglion sensory and sympathetic neurons. | Nerve growth factor (NGF)-stimulated neurite outgrowth in the rat PC12 tumor cell line recently has been shown to depend on the activation of the mitogen-activated protein (MAP) kinase kinase 1 (MEK1) (Pang et al.: J Biol Chem 270:13585-13588; 1995). In this study we have analyzed whether or not function of the MAP kinase pathway is necessary for NGF-stimulated neurite outgrowth in two subtypes of primary neurons derived from the embryonic chick peripheral nervous system (PNS). Treatment of p21ras-dependent | 8978506 | [
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Nerve growth factor-stimulated mitogen-activated protein kinase activity is not necessary for neurite outgrowth of chick dorsal root ganglion sensory and sympathetic neurons. | dorsal root ganglion (DRG) sensory neurons (E9) with the MEK1 inhibitor PD98059 at concentrations up to 100 microM did not prevent NGF-stimulated neurite outgrowth. At this concentration NGF-stimulated tyrosine phosphorylation of MAP kinase p42 as well as MAP kinase activity both were decreased by approximately 80%. Essentially the same results were obtained with p21ras-independent sympathetic neurons (E12). We conclude that; in contrast to the PC12 tumor cell line; NGF-stimulated MAP kinase activity is no | 8978506 | [
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