Search results for " LDL"

showing 10 items of 454 documents

Homozygous familial hypobetalipoproteinemia: two novel mutations in the splicing sites of apolipoprotein B gene and review of the literature.

2015

Objective: Familial hypobetalipoproteinemia (FHBL) is autosomal codominant disorder of lipoprotein metabolism characterized by low plasma levels of total cholesterol (TC), low-density lipoproteincholesterol (LDL-C) and apolipoprotein B (apoB) below the 5 th percentile of the distribution in the population. Patients with the clinical diagnosis of homozygous FHBL (Ho-FHBL) are extremely rare and few patients have been characterized at the molecular level. Here we report the medical history and the molecular characterization of one paediatric patient with clinical features of Ho-FHBL. Methods: A one month old infant with failure to thrive, severe hypocholesterolemia and acanthocytosis was clin…

ProbandAdultMaleAcanthocytosiSettore MED/09 - Medicina InternaApolipoprotein BPopulationDNA Mutational AnalysisBiologyHypobetalipoproteinemiasExonHumanseducationGeneGeneticseducation.field_of_studyHomozygoteIntronInfantCholesterol LDLAbetalipoproteinemiaIntronsAlternative SplicingHomozygous familial hypobetalipoproteinemiaCholesterolRNA splicingApolipoprotein B-100Mutationbiology.proteinlipids (amino acids peptides and proteins)FemaleCardiology and Cardiovascular MedicineApolipoprotein BMinigeneAtherosclerosis
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Genetic diagnosis of familial hypercholesterolemia in a South European outbreed population: influence of low-density lipoprotein (LDL) receptor gene …

2001

The aims of this study were to examine the presence of mutations in the low-density lipoprotein receptor gene among subjects clinically diagnosed with familial hypercholesterolemia and to analyze whether the molecular diagnosis helps to predict the response to simvastatin treatment in our familial hypercholesterolemia population. Fifty-five probands and 128 related subjects with familial hypercholesterolemia were studied. Genetic diagnosis was carried out following a three-step protocol based on Southern blot and PCR-single strand conformational polymorphism analysis. A randomized clinical trial with simvastatin was conducted in 42 genetically diagnosed subjects with familial hypercholester…

ProbandAdultMalemedicine.medical_specialtySimvastatinEndocrinology Diabetes and MetabolismClinical BiochemistryPopulationFamilial hypercholesterolemiaBiologyBiochemistryHyperlipoproteinemia Type IIchemistry.chemical_compoundEndocrinologyHigh-density lipoproteinApolipoproteins EInternal medicinemedicineHumanseducationAgedApolipoproteins Beducation.field_of_studyCholesterolBiochemistry (medical)Cholesterol HDLnutritional and metabolic diseasesCholesterol LDLMiddle Agedmedicine.diseaseEndocrinologychemistryReceptors LDLSimvastatinLow-density lipoproteinMutationlipids (amino acids peptides and proteins)FemaleHydroxymethylglutaryl-CoA Reductase InhibitorsLipoproteinmedicine.drugThe Journal of clinical endocrinology and metabolism
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Additive effect of mutations in LDLR and PCSK9 genes on the phenotype of familial hypercholesterolemia.

2006

Patients homozygous or Compound heterozygous for LDLR mutations or double heterozygous for LDLR and apo B R3500Q mutation have higher LDL-C levels. more extensive xanthomatosis and more severe premature coronary disease (pCAD) than simple heterozygotes for mutations in either these genes or for missense mutations in PCSK9 gene. It is not known whether combined mutations in LDLR and PKCS9 are associated with such a severe phenotype. We sequenced Apo B and PCSK9 genes in two patients with the clinical diagnosis of homozygous FH who were heterozygous for LDLR gene mutations. Proband Z.P. (LDL-C 13.39 mmol/L and pCAD) was heterozygous for an LDLR mutation (p.E228K) inherited from her father (LD…

ProbandLDLR geneAdultMaleSettore MED/09 - Medicina InternaApolipoprotein BFamilial hypercholesterolemia (FH); Autosomal dominant hypercholesterolemia 3 (ADH3); LDLR gene; PCSK9 gene; Premature coronary artery diseasePremature coronary artery diseaseLDLR PCSK9Mutation MissenseFamilial hypercholesterolemiaCompound heterozygositymedicine.disease_causeHyperlipoproteinemia Type IIFamilial hypercholesterolemia (FH) Autosomal dominant hypercholesterolemia 3 (ADH3) LDLR gene PCSK9 gene Premature coronary artery diseaseFamilial hypercholesterolemia (FH)medicineMissense mutationHumansCells CulturedGeneticsMutationbiologybusiness.industrySerine EndopeptidasesHeterozygote advantageMiddle Agedmedicine.diseaseAutosomal dominant hypercholesterolemia 3 (ADH3)PedigreePhenotypeSettore MED/03 - Genetica MedicaAmino Acid SubstitutionReceptors LDLPCSK9 geneLDL receptorbiology.proteinlipids (amino acids peptides and proteins)FemaleProprotein ConvertasesProprotein Convertase 9Cardiology and Cardiovascular MedicinebusinessAtherosclerosis
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Lack of phenotypic additive effect of familial defective apolipoprotein B3531 in familial hypercholesterolaemia.

2020

Familial defective apolipoprotein (apo) B (FDB) and familial hypercholesterolaemia (FH) are the two common genetic conditions that cause hypercholesterolaemia. R3531C mutation of the APOB gene is a rare cause of FDB. Individuals with both FDB and FH are rare. A 51-year-old man with hypercholesterolaemia (11.4 mmol/L) and his family were studied. Low-density lipoprotein (LDL) receptor (LDLR) and APOB genes were analysed by direct sequencing. LDL of four subjects were studied in a fibroblast LDL receptor-binding displacement assay. We found a mutation of the LDLR gene (p.Y398X) in the proband and in four other family members: the p.R3531C APOB gene mutation was also found in the proband, his …

ProbandMalemedicine.medical_specialtyApolipoprotein B030204 cardiovascular system & hematologyCompound heterozygosityHyperlipoproteinemia Type II03 medical and health scienceschemistry.chemical_compoundFDB35310302 clinical medicineInternal medicineInternal MedicinemedicineHumans030212 general & internal medicineApolipoproteins Bdouble heterozygotebiologybusiness.industryCholesterolLDL receptornutritional and metabolic diseasesHeterozygote advantageMiddle AgedEndocrinologychemistryItalyReceptors LDLLDL receptorMutation (genetic algorithm)Mutationfamilial hypercholesterolaemiabiology.proteinlipids (amino acids peptides and proteins)businessLipoproteinInternal medicine journalReferences
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Fatty acids liberated from low-density lipoprotein trigger endothelial apoptosis via mitogen-activated protein kinases.

2005

Enzymatic modification of low-density lipoprotein (LDL) as it probably occurs in the arterial intima drastically increases its cytotoxicity, which could be relevant for the progression of atherosclerotic lesions. LDL was treated with a protease and cholesterylesterase to generate a derivative similar to lesional LDL, with a high content of free cholesterol and fatty acids. Exposure of endothelial cells to the enzymatically modified lipoprotein (E-LDL), but not to native or oxidized LDL, resulted in programmed cell death. Apoptosis was triggered by apoptosis signal-regulating kinase 1 dependent phosphorylation of p38. Depletion and reconstitution experiments identified free fatty acids (FFA)…

Programmed cell deathp38 mitogen-activated protein kinasesBlotting WesternApoptosisDNA FragmentationBiologyFatty Acids NonesterifiedMAP Kinase Kinase Kinase 5p38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundHumansPhosphorylationMolecular BiologyCells CulturedCaspase 7Cell growthKinaseCaspase 3Cell BiologyCell biologyLipoproteins LDLchemistryBiochemistryApoptosisLow-density lipoproteinCaspasesPhosphorylationlipids (amino acids peptides and proteins)Endothelium VascularLipoproteinOleic AcidCell death and differentiation
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Enzymatically modified LDL induces cathepsin H in human monocytes: potential relevance in early atherogenesis.

2003

Objective—Modification with proteases and cholesterylesterase transforms LDL to a moiety that resembles lipoproteins isolated from atherosclerotic lesions and possesses atherogenic properties. To identify changes in monocyte-derived foam cells laden with enzymatically modified LDL (E-LDL), we compared patterns of the most abundant transcripts in these cells after incubation with LDL or E-LDL.Methods and Results—Serial analyses of gene expression (SAGE) libraries were constructed from human monocytes after treatment with LDL or E-LDL. Several tags were differentially expressed in LDL-treated versus E-LDL–treated cells, whereby marked selective induction by E-LDL of cathepsin H was conspicuou…

ProteasesCathepsin HCoronary Artery DiseaseBiologyCathepsin HCathepsin L1medicineMacrophageHumansFoam cellGene LibraryCathepsinMonocyteGene Expression ProfilingColocalizationSterol EsteraseMolecular biologyCathepsinsLipoproteins LDLCysteine Endopeptidasesmedicine.anatomical_structureCholesterolBiochemistryGene Expression Regulationlipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineFoam CellsArteriosclerosis, thrombosis, and vascular biology
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Statins and peripheral arterial disease: effects on claudication, disease progression, and prevention of cardiovascular events.

2006

Peripheral arterial disease (PAD) of the lower limbs is the third most important site of atherosclerotic disease alongside coronary heart disease (CHD) and cerebrovascular disease (CVD). Best medical treatment is beneficial even in patients who eventually need invasive treatment, as the safety, immediate success, and durability of intervention is greatly improved in patients who adhere to best medical treatment. In recent years, a number of studies have suggested that the ACE-inhibitor ramipril and different statins, together with antiplatelet drugs, reduce cardiovascular morbidity and mortality in PAD. Patients with PAD are really a category of patients with a very high cardiovascular risk…

Ramiprilmedicine.medical_specialtyRenal functionCoronary Diseasechemistry.chemical_compoundRisk FactorsInternal medicinemedicineHumanscardiovascular diseasesPeripheral Vascular DiseasesFramingham Risk ScoreCholesterolbusiness.industryAnticholesteremic AgentsGeneral MedicineArteriesCholesterol LDLIntermittent ClaudicationAtherosclerosisIntermittent claudicationPeripheralchemistryHemostasisCardiologyDisease Progressionmedicine.symptomHydroxymethylglutaryl-CoA Reductase InhibitorsClaudicationbusinessmedicine.drugArchives of medical research
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Targeting of biotinylated compounds to its target tissue using a low-density lipoprotein receptor–avidin fusion protein

2003

The very high binding affinity of avidin to biotin is one of the highest to occur in nature. We constructed a fusion protein composed of avidin and the endocytotic LDL receptor in order to target biotinylated molecules to cells of the desired tissues. In addition to the native avidin, charge-mutated and nonglycosylated avidins were utilized as part of the fusion proteins, in order to modify its properties. All of the fusion protein versions retained the biotin-binding capacity. Although the specificity was not increased, however, fusion proteins composed of natural avidin and nonglycosylated avidin bound most efficiently to the biotinylated ligands. Fluorescence microscopy and atomic force …

Recombinant Fusion ProteinsBlotting WesternGenetic VectorsBiotinBiologyCell FractionationMicroscopy Atomic ForceCell membranechemistry.chemical_compoundBiotinGeneticsFluorescence microscopemedicineAnimalsMolecular BiologyBrain NeoplasmsCell MembraneGenetic TherapyGliomaAvidinLigand (biochemistry)Semliki forest virusFusion proteinRatsmedicine.anatomical_structureMicroscopy FluorescenceReceptors LDLchemistryBiochemistryBiotinylationGene TargetingLDL receptorbiology.proteinMolecular MedicineAvidinGene Therapy
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Effect of a 1-year elastic band resistance exercise program on cardiovascular risk profile in postmenopausal women

2018

Objective: The aim of this study was to investigate the effects of a 1-year progressive resistance training program using elastic bands on cardiovascular profile parameters in sedentary postmenopausal (>12 months’ amenorrhea) women. Methods: This longitudinal prospective experimental study included 38 menopausal women who were randomly divided into two groups: an intervention group (IG, n = 18), who completed a progressive resistance training program with elastic bands over the course of 12 months (six exercises for whole body training, three sets × 10 repetitions), and a control group (CG, n = 20) that did not perform any training. Blood analysis and body composition were determined at bas…

Riskmedicine.medical_specialtyWaist030204 cardiovascular system & hematologyBody compositionStatistics NonparametricC-reactive protein03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRisk FactorsInternal medicineEducación Física y DeportivamedicineHumansLongitudinal StudiesProspective StudiesProspective cohort studyTriglyceridesAgedAnalysis of Variancemedicine.diagnostic_testbiologyCholesterolbusiness.industryBody WeightC-reactive proteinObstetrics and GynecologyResistance TrainingCholesterol LDL030229 sport sciencesAnthropometryCircumferenceResistance trainingPostmenopauseC-Reactive ProteinCholesterolchemistryCardiovascular DiseasesBody Compositionbiology.proteinFemaleAmenorrheaWaist Circumferencemedicine.symptomLipid profilebusinessFollow-Up StudiesMenopause
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ApoE polymorphism in a small Mediterranean island: Relationships with plasma lipids, lipoproteins and LDL particle size

2001

Polymorphisms of apoE gene are able to modulate lipoprotein metabolism at different steps and to influence LDL-cholesterol (LDL-C) levels and also other lipoproteins features. Population studies documented large differences in the frequency of apoE alleles which could be even related to the prevalence of cardiovascular disease. In this study we evaluated the apoE genotypes and allele frequency in 576 subjects living in a small island in the Tyrrhenian Sea and the relative contribution of apoE polymorphism on plasma lipid and lipoprotein profile, including LDL particle size. We found a cumulative frequency of 0.073, 0.866 and 0.061 for ε2, ε3 and ε4 alleles respectively. Moreover ε3 subjects…

Settore MED/09 - Medicina InternaApoE gene Lipoproteins LDL particle size Mediterranean population
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