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  • 1
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    An apolipoprotein influencing triglycerides in humans and mice revealed by comparative sequencing (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-10-06
    Description: Comparison of genomic DNA sequences from human and mouse revealed a new apolipoprotein (APO) gene (APOAV) located proximal to the well-characterized APOAI/CIII/AIV gene cluster on human 11q23. Mice expressing a human APOAV transgene showed a decrease in plasma triglyceride concentrations to one-third of those in control mice; conversely, knockout mice lacking Apoav had four times as much plasma triglycerides as controls. In humans, single nucleotide polymorphisms (SNPs) across the APOAV locus were found to be significantly associated with plasma triglyceride levels in two independent studies. These findings indicate that APOAV is an important determinant of plasma triglyceride levels, a major risk factor for coronary artery disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennacchio, L A -- Olivier, M -- Hubacek, J A -- Cohen, J C -- Cox, D R -- Fruchart, J C -- Krauss, R M -- Rubin, E M -- HL-18574/HL/NHLBI NIH HHS/ -- HL-53917/HL/NHLBI NIH HHS/ -- HL66681/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2001 Oct 5;294(5540):169-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genome Sciences Department, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11588264" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Alleles ; Animals ; Apolipoprotein C-III ; Apolipoproteins/*genetics/*physiology ; Apolipoproteins A ; Apolipoproteins C/blood ; Chromosomes, Human, Pair 11 ; Cohort Studies ; Computational Biology ; Coronary Disease/etiology/genetics ; Expressed Sequence Tags ; Female ; Haplotypes ; Humans ; Linkage Disequilibrium ; Lipoproteins, VLDL/blood ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Multigene Family ; Open Reading Frames ; Polymorphism, Single Nucleotide ; Risk Factors ; Sequence Analysis, DNA ; Transgenes ; Triglycerides/*blood
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Protection against atherogenesis in mice mediated by human apolipoprotein A-IV (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-16
    Description: Apolipoproteins are protein constituents of plasma lipid transport particles. Human apolipoprotein A-IV (apoA-IV) was expressed in the liver of C57BL/6 mice and mice deficient in apoE, both of which are prone to atherosclerosis, to investigate whether apoA-IV protects against this disease. In transgenic C57BL/6 mice on an atherogenic diet, the serum concentration of high density lipoprotein (HDL) cholesterol increased by 35 percent, whereas the concentration of endogenous apoA-I decreased by 29 percent, relative to those in transgenic mice on a normal diet. Expression of human apoA-IV in apoE-deficient mice on a normal diet resulted in an even more severe atherogenic lipoprotein profile, without affecting the concentration of HDL cholesterol, than that in nontransgenic apoE-deficient mice. However, transgenic mice of both backgrounds showed a substantial reduction in the size of atherosclerotic lesions. Thus, apoA-IV appears to protect against atherosclerosis by a mechanism that does not involve an increase in HDL cholesterol concentration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duverger, N -- Tremp, G -- Caillaud, J M -- Emmanuel, F -- Castro, G -- Fruchart, J C -- Steinmetz, A -- Denefle, P -- New York, N.Y. -- Science. 1996 Aug 16;273(5277):966-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rhone-Poulenc Rorer, Gencell Division, Atherosclerosis Department, Centre de Recherches de Vitry-Alfortville, 94403 Vitry sur Seine Cedex, France. G. C.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8688083" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoprotein A-I/blood ; Apolipoproteins A/blood/*physiology ; Apolipoproteins E/blood/deficiency ; Arteriosclerosis/*prevention & control ; Cholesterol/blood ; Cholesterol, HDL/blood ; Diet, Atherogenic ; Female ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
    Electronic Resource
    Electronic Resource
    An update on the mechanisms of action of the peroxisome proliferator-activated receptors (PPARs) and their roles in inflammation and cancer (1999)
    Springer
    Cellular and molecular life sciences 55 (1999), S. 932-943 
    Details
    ISSN: 1420-9071
    Keywords: Key words. PPAR; nuclear receptor; lipid homeostasis; cofactor; inflammation; tumorigenesis; apoptosis.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors and have been initially described as molecular targets for compounds which induce peroxisome proliferation. The interest of researchers for PPARs increased dramatically when these receptors were shown to be directly activated by a number of medically relevant compounds. These compounds include: the fibrate class of hypolidemic drugs, the thiazolidinediones, which are insulin sensitizers used as orally active antidiabetic agents, certain non-steroidal anti-inflammatory drugs (NSAIDs), and naturally occurring fatty acid-derived molecules. Rapidly, it was demonstrated that PPARs are key regulators of lipid homeostasis and provide a molecular link between nutrition and gene regulation. Recently, detailed studies of PPAR expression profiles in different tissues pointed to the roles these receptors play in inflammation control and cell proliferation. In this review we will focus on the new insights gained into these two areas and we will also discuss our current knowledge of the regulation of PPAR transcriptional activity by cofactors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000180050345
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  • 4
    Electronic Resource
    Electronic Resource
    The polymorphism ApoB/4311 in patients with myocardial infarction and controls: the ECTIM study (1992)
    Springer
    Human genetics 〈Berlin〉 89 (1992), S. 169-175 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The polymorphism affecting codon 4311 of the apolipoprotein B gene (ApoB/4311) was investigated in a large case-control study in two French and one Northern Irish geographically defined populations. Cases were recruited 3 to 9 months after a myocardial infarction (MI) and controls were randomly selected from the population. The polymorphism was assessed using allele-specific oligonucleotides (ASO). The genotype frequencies of the ApoB/4311 polymorphism did not differ in Northern Ireland and France and were in Hardy-Weinberg equilibrium in all groups; strong associations with three other polymorphisms of the ApoB gene (XbaI, EcoRI, VNTR(34 repeats)) were observed and it was possible to identify highly sensitive and specific markers of the ApoB/4311 rare variant. Homozygotes for the ApoB 4311 rare variant were slightly less frequent in cases than in controls: 22 (4.4%) and 35 (6.7%) respectively (population adjusted χ2=3.3 P〈0.07), especially in Belfast: 6 (3.1%) and 12 (7.6%), respectively (P〈0.06). Several lipid and lipoprotein parameters were measured. Consistently among control groups, rare homozygotes had lower mean levels of ApoB (P〈0.02), triglycerides (P〈0.02), and lipoprotein particles containing ApoE and ApoB (LpE:B; P〈0.001) and a higher mean level of lipoprotein particles containing ApoAI and not ApoAII (LpAI; P〈0.02) than heterozygotes and frequent homozygotes combined. The strong association between the ApoB/4311 polymorphism and LpE:B was also observed in patients with MI. When present in the homozygous form, the ApoB/ 4311 Asn→Ser variant is associated with a lipoprotein profile that is apparently favourable.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00217118
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  • 5
    Electronic Resource
    Electronic Resource
    Apolipoprotein B signal peptide polymorphism in patients with myocardial infarction and controls (1993)
    Springer
    Human genetics 〈Berlin〉 90 (1993), S. 561-565 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract We report the allele frequencies of the apolipoprotein B (Apo B) signal peptide polymorphism in patients with myocardial infarction and compare them with controls. The first sample consists of 197 myocardial infarction patients and 168 controls from Belfast (UK). The second sample consists of 167 myocardial infarction patients and 205 controls from Strasbourg (France), and the third consists of 71 patients and 146 controls from Haute-Garonne (Toulouse, France). No significant differences were observed in the frequency distribution of genotypes among cases and controls or between populations. However, there were more rare homozygotes in the Belfast cases. Significant associations were observed between the Apo B signal peptide polymorphism and mean levels of total cholesterol, low density lipoprotein cholesterol, Apo B and lipoprotein particles containing Apo (a) [Lp(a)] in the Strasbourg control population. Individuals homozygous for the rare allele had higher levels of these lipid parameters. In Belfast, although not statistically significant, the Apo B signal peptide polymorphism had a similar effect on Apo-B-related parameters as seen in Strasbourg. No significant associations were observed in the Haute-Garonne population where the risk of myocardial infarction is three times lower than in Belfast. In all three populations, the average Lp(a) levels were consistently different among Apo B signal peptide genotypes. These data implicate the Apo B signal peptide in determining some of the risks of myocardial infarction in these populations. Regardless of the exact mechanism, the Apo B signal peptide is an important candidate locus for the study of potentially atherogenic lipid variants.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00217459
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  • 6
    Electronic Resource
    Electronic Resource
    Polymorphisms of the apolipoprotein B and E genes and their relationship to plasma lipid variables in healthy Chinese men (1993)
    Springer
    Human genetics 〈Berlin〉 92 (1993), S. 191-197 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract In this study we have analysed the apolipoprotein (Apo) E polymorphism and polymorphisms of the ApoB gene, including the ApoB/Xba I and ApoB/4311 diallelic polymorphisms and a hypervariable region (HVR) situated in the 3′ region of the gene (ApoB/3′HVR), in a sample of healthy male subjects from Taiyuan (northern People's Republic of China). In comparison to Caucasian populations, in the Chinese sample, the Xba I2 allele (presence of cutting site; frequency 6.1%; and 95% confidence interval, 3.3–8.9) and the long HVR alleles (9.4%; 6.0–12.8) were rare, whereas the ApoB/4311 (Ser) allele (70.8%; 65.4–76.2) and the 34-repeat allele of the HVR (HVR34; 62.4%; 56.8–68.0) were frequent. In subjects having none, one, or two HVR34 alleles, the mean levels of plasma triglycerides were 2.32±1.44 (SD), 1.45+0.74, and 1.75±1.07 g/l, respectively (P 〈 0.007). Similar trends were observed for very low density lipoprotein (VLDL) cholesterol, LpE:B, and LpCIII:B. The frequencies of the ApoE alleles were similar to those reported in other populations of Asian origin; E2 (7.4%; 4.2–10.6), E3 (84.4%; 80.2–88.6), and E4 (8.2%; 5.0–11.4). Individuals carrying the E2 allele had a lower mean level of ApoB than E33 individuals: 0.87±0.16 and 1.00±0.22 g/l, respectively (P 〈 0.007). Individuals carrying the E4 allele had higher levels of ApoE than E33 individuals: 0.140±0.084 and 0.094±0.052 g/l, respectively (P 〈 0.004); similar trends were observed for VLDL cholesterol, triglycerides, LpE:B, and LpCIII:B. The ApoB/ HVR34 and ApoE/E4 polymorphisms accounted for 10% to 15% of the variability of the plasma levels of VLDL cholesterol, ApoE, triglycerides, LpE:B, and LpCIII:B. Several lipid variables appeared to be favourably affected by specific forms of ApoB and ApoE that are particularly frequent in this Chinese population.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00219691
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  • 7
    Electronic Resource
    Electronic Resource
    Effect of simvastatin on plasma lipids, apolipoproteins and lipoprotein particles in patients with primary hypercholesterolaemia (1989)
    Springer
    European journal of clinical pharmacology 37 (1989), S. 545-550 
    Details
    ISSN: 1432-1041
    Keywords: simvastatin ; hypercholesterolaemia ; HMG-CoA reductase inhibitor ; cholesterol ; apolipoproteins ; lipoprotein particles
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effect of treatment with simvastatin, a new HMG-CoA reductase inhibitor, has been investigated in 27 patients with primary hypercholesterolaemia. It produced a significant decrease of cholesterol and phospholipids in plasma, LDL and apolipoprotein B-containing lipoproteins. Plasma apolipoproteins B, C-III and E were also significantly lowered. The concentration of lipoprotein particles recognized by monoclonal antibodies (BL3, BL5 and BL7), associated with atherosclerotic disease, was also lowered by the treatment. Lipoproteins LpA-II:A-I were not changed, while LpA-I, which has been suggested to be the protective fraction of the apo A-I-containing lipoproteins, was slightly and inconsistently increased.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00562541
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  • 8
    Electronic Resource
    Electronic Resource
    Efficacy and safety of high dose fluvastatin in patients with familial hypercholesterolaemia (1993)
    Springer
    European journal of clinical pharmacology 45 (1993), S. 513-518 
    Details
    ISSN: 1432-1041
    Keywords: Hypercholesterolaemia ; Fluvastatin ; molecular genetics ; LDL receptor ; hyperlipidaemia ; atherosclerosis ; HMG CoA reductase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The efficacy and safety of the HMG CoA reductase inhibitor fluvastatin have been evaluated in a double blind study in 52 patients with familial hypercholesterolaemia. A standard AHA Phase II lipid lowering diet was prescribed throughout the study. After 6 weeks of a single blind dosage stabilisation period, in which patients received fluvastatin 40 mg qPM, patients were randomly allocated to one of two double blind treatment groups: group A (n=24) received fluvastatin 20 mg b. d. for 12 weeks and fluvastatin 20 mg AM + 40 mg PM for an additional 12 weeks; Group B (n=28) received fluvastatin 40 mg qPM during the entire study. Safety and tolerability were evaluated by the analysis of biochemical and haematological parameters, and ophthalmological and physical examinations. Efficacy was analysed by the determination of plasma lipids, lipoproteins and apoproteins. Fluvastatin 40 mg/d was associated with up to a 27.4% decrease in LDL-C and a 9.6% increase in HDL-C concentrations. Increasing the dose of fluvastatin from 20 mg b. d. to 60 mg per day in Group A was associated with a 7.1% decrease in LDL-C, a 12.1% increase of HDL-C and a 12.8% decrease in the LDL-C/HDL-C ratio. In comparison with Group B (40 mg qPM) LDL-C, HDL-C and the LDL-C/HDL-C ratio in Group A (60 mg) differed by −8.9%, 6.6% and −12%, respectively. During treatment with 40 mg qPM, one patient developed an asymptomatic but notable elevation of CK to 1823 U/l (normal range 0–100 U/l) that was caused by strenuous exercise. No other notable biochemical or haematological abnormalities were recorded. It is concluded that in patients with heterozygous FH the increase of fluvastatin from 40 to 60 mg/d provided an additional significant effect on plasma LDL-C and HDL-C levels and in the LDL-C/HDL-C ratio, without producing any deleterious effect.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00315307
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  • 9
    Electronic Resource
    Electronic Resource
    Fluvastatin efficacy and tolerability in comparison and in combination with cholestyramine (1994)
    Springer
    European journal of clinical pharmacology 46 (1994), S. 445-449 
    Details
    ISSN: 1432-1041
    Keywords: Hypercholesterolaemia ; Fluvastatin ; cholestyramine ; drug treatment of hypercholesterolaemia ; LDL cholesterol ; HDL cholesterol ; triglycerides ; Lp(a) ; apolipoproteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract The aim of this study was to investigate the new synthetic HMG-CoA reductase inhibitor, fluvastatin, for efficacy, safety and tolerability in comparison to cholestyramine. One hundred fifty one primary hypercholesterolaemic patients participated in this double-blind, parallel-group, randomized study. During the first 12 weeks of the study, fluvastatin (20 mg and 40 mg daily) was compared with cholestyramine (16 g per day). In the subsequent, 6-week part of the study, the comparative efficacy, safety and tolerability of 20 mg fluvastatin, combined with cholestyramine (4 g, 8 g, or 16 g) were assessed. Fluvastatin (40 mg) reduced LDL cholesterol by 28.0%, triglycerides by 10.5% and increased HDL cholesterol by 3.7%. Cholestyramine (16 g) reduced LDL cholesterol by 35.0%, but raised triglycerides and HDL cholesterol by 12.3% (p〈0.01) and 3.7% respectively. The combination of fluvastatin 20 mg and cholesty-ramine (4 g, 8 g and 16 g) induced the following reductions in LDL cholesterol: 30.4%, 35.6% and 46.6% respectively. There was no significant change in triglycerides in either group although HDL cholesterol was raised by 4.9%, 8.3% and 7.2% respectively. One patient treated with fluvastatin and two treated with cholesty-ramine were withdrawn from the study due to elevation of liver transaminases. The most frequent subjective adverse effects in both treatment groups were mild, transient gastrointestinal complaints. Thus, fluvastatin was effective as a lipid-lowering agent; the effect was further enhanced when fluvastatin was combined with cholestyramine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00191909
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  • 10
    Electronic Resource
    Electronic Resource
    Antioxidant Therapy and Uptake of Human Oxidized LDL by Macrophages (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 570 (1989), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1989.tb14953.x
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