Search results for "LDL"

showing 10 items of 664 documents

Rapid screening of the LDL receptor point mutation FH-Genoa/Palermo

1999

The LDL-receptor gene point mutation FH-Genoa/Palermo is the most frequent mutation responsible for Familial Hypercholesterolemia in Sicily. The mutation does not introduce or abolish any useful restriction site. We establish a GeneComb™-based strategy to identify this mutation in a population of Sicilian unrelated clinically diagnosed FH probands. The method was very sensitive and specific; 12 out of 90 (13.3%) unrelated FH probands were found to carry the FH-Genoa/Palermo mutation. According to these results, the FH-Genoa/Palermo is the more frequent LDL-receptor gene mutation among the Sicilian FH patients. Moreover FH-Genoa/Palermo is the mutation cluster to date more represented in Sou…

ProbandGeneticseducation.field_of_studyPoint mutationPopulationFamilial hypercholesterolemiaGene mutationBiologymedicine.diseaseRestriction siteMutation (genetic algorithm)LDL receptorGeneticsmedicineeducationGenetics (clinical)Human Mutation
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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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The era of reference genomes in conservation genomics

2022

Progress in genome sequencing now enables the large-scale generation of reference genomes. Various international initiatives aim to generate reference genomes representing global biodiversity. These genomes provide unique insights into genomic diversity and architecture, thereby enabling comprehensive analyses of population and functional genomics, and are expected to revolutionize conservation genomics.

QH301 Biology580 Plants (Botany)Genetics -- ResearchEvolutionsbiologibiodiversity conservation; conservation genetics; ERGA; European Reference Genome AtlasConservation genetics; Biodiversity conservation; European Reference Genome Atlas; ERGAAnimal genome mappingudc:630*1GenomeGEERGA[SDV.BID.EVO]Life Sciences [q-bio]/Biodiversity/Populations and Evolution [q-bio.PE][SDE.BE.BIOD]Environmental Sciences/Biodiversity and Ecology/domain_sde.be.biodERGA ; Biodiversity [MeSH] ; Genomics [MeSH] ; Ecology Evolution Behavior and Systematics ; conservation genetics ; Genome [MeSH] ; biodiversity conservation ; European Reference Genome Atlas3rd-DASGenomicsBiodiversityreferenčni genomi[SDV.BIBS]Life Sciences [q-bio]/Quantitative Methods [q-bio.QM][SDE.BE.BEC]Environmental Sciences/Biodiversity and Ecology/domain_sde.be.becChemistry10121 Department of Systematic and Evolutionary BotanygenomikaGE Environmental Sciences:Informàtica::Aplicacions de la informàtica::Bioinformàtica [Àrees temàtiques de la UPC]biodiverzitetaSettore BIO/18 - GENETICAeducationQH426 GeneticsQH301European Reference Genome AtlasVDP::Matematikk og Naturvitenskap: 400::Basale biofag: 470[SDE.BE.EVO]Environmental Sciences/Biodiversity and Ecology/domain_sde.be.evoGeneticsconservation genetics ; biodiversity conservation ; European Reference Genome Atlas ; ERGAgenomi10211 Zurich-Basel Plant Science CenterGenomesGenetikBiologyQH426Ecology Evolution Behavior and SystematicsEvolutionary BiologyBiodiversity conservation; Conservation genetics; European Reference Genome AtlasAmbientaleEcologíaGenética1105 Ecology Evolution Behavior and Systematicsconservation geneticsWildlife conservation570 Life sciences; biologyHuman medicinebiodiversity conservationAnimal genetics[SDE.BE]Environmental Sciences/Biodiversity and EcologyGenètica
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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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Holidays? Not for all. Eagles have larger home ranges on holidays as a consequence of human disturbance

2019

Human-wildlife conflicts are the object of raising concern in conservation biology. People living in urban areas are rapidly increasing worldwide and consequently the temporal pattern of occupation of natural areas for recreation is changing as well, resulting in an ever-increasing concentration of people during weekends and holidays. This is particularly evident in affluent societies, where more recreationists visit natural areas on holidays and weekends, causing disturbance to wildlife in the so-called “weekend effect”. Here, we tested the response to disturbance of 30 Bonelli's eagles tracked by high-frequency GPS/GSM telemetry. We analysed daily home-range size, a measure of changing be…

Recreational activities0106 biological sciencesRaptorsWeekend effectGPS010604 marine biology & hydrobiologyWildlifeConservationAnnual cycleOutdoor activities010603 evolutionary biology01 natural sciencesGeographyNestDisturbance (ecology)Human disturbanceSpace useTelemetryZoologíaConservation biologySocioeconomicsQuality informationRecreationEcology Evolution Behavior and SystematicsNature and Landscape ConservationBiological Conservation
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Mboat7 down-regulation by hyper-insulinemia induces fat accumulation in hepatocytes.

2020

Background: Naturally occurring variation in Membrane-bound O-acyltransferase domain-containing 7 (MBOAT7), encoding for an enzyme involved in phosphatidylinositol acyl-chain remodelling, has been associated with fatty liver and hepatic disorders. Here, we examined the relationship between hepatic Mboat7 down-regulation and fat accumulation. Methods: Hepatic MBOAT7 expression was surveyed in 119 obese individuals and in experimental models. MBOAT7 was acutely silenced by antisense oligonucleotides in C57Bl/6 mice, and by CRISPR/Cas9 in HepG2 hepatocytes. Findings: In obese individuals, hepatic MBOAT7 mRNA decreased from normal liver to steatohepatitis, independently of diabetes, inflammatio…

Research paperTGFβ Transforming Growth Factor BetaIntracellular SpaceCRISPR Clustered Regularly Interspaced Short Palindromic RepeatshHEPS Human HepatocytesMice0302 clinical medicineLPIAT1DAG Diacylglyceroli.p. Intraperitonealmedia_commonFatty AcidsGeneral Medicine3. Good health030220 oncology & carcinogenesisHOMA-IR homeostasis Model Assessment of Insulin ResistanceMPO morpholinolcsh:Medicine (General)medicine.medical_specialtyPE Phosphatidyl-EthanolamineNashGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesTNFα tumor Necrosis Factor AlphaLDL Low Density LipoproteinsHyperinsulinismNAFLDSD Standard Dietmedia_common.cataloged_instanceHumansCPT1 Carnitine Palmitoyltransferase IPhosphatidylinositolGene SilencingEuropean unionVLDL Very Low Density Lipoproteinlcsh:RhHSC Human Hepatic Stellate Cellsmedicine.diseaseLipid MetabolismOA Oleic AcidCI Confidence IntervalMboat7 Membrane bound O-acyltransferase domain containing 7MCD methionine choline deficient diet030104 developmental biologyEndocrinologychemistryCDP Cytidine-DiphosphateFOXO1 Forkhead Box protein O1NAFLD nonalcoholic fatty liver diseaseSteatohepatitisBMI Body Mass IndexCL CardiolipinAcyltransferases0301 basic medicineAlcoholic liver diseaseCXCL10 C-X-C Motif Chemokine 10lcsh:Medicinechemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseIFG Impaired Fasting GlucoseAPOB Apolipoprotein BNonalcoholic fatty liver diseasePIP Phosphatidyl-Inositol-PhosphateSteatohepatitisqRT-PCR quantitative Real Time Polymerase Chain ReactionMice Knockoutlcsh:R5-920ORO Oil Red O StainingPI PhosphatidylinositolFatty liverTM6SF2 Transmembrane 6 Superfamily Member 2PhospholipidTAG TriglyceridesNASH Nonalcoholic SteatohepatitisLipogenesisLPA Lyso-Phosphatidic AcidPhosphatidylinositolSignal TransductionPS Phosphatidyl-SerinePA Palmitic AcidALD alcoholic liver diseasePC Phosphatidylcholinei.v. IntravenousFATP1 Fatty Acid Transport Protein 1Models BiologicalInternal medicinemedicineAnimalsNonalcoholic fatty liver diseasePPARα Peroxisome Proliferator-Activated Receptor alphaObesityG3P Glyceraldehyde-3-PhosphateSREBP1c Sterol Regulatory Element-Binding Protein 1HDL High Density Lipoproteinsbusiness.industryPI3K Phosphatidylinositol 3 KinaseMembrane ProteinsNHEJ Non-Homologues End JoiningPNPLA3 Patatin-like Phospholipase Domain-containing-3MTTP Microsomal Triglyceride Transfer ProteinLPIAT1 Lysophosphatidylinositol Acyltransferase 1TMC4 Transmembrane Channel-Like 4Disease Models AnimalGene Expression RegulationHepatocytesFOXA2 Forkhead Box A2mTOR mammalian target of RapamycinSteatosisInsulin ResistancebusinessPG Phosphatidyl-GlycerolFABP1 Fatty Acid-Binding Protein 1 FAS Fatty Acid SynthaseT2DM Type 2 Diabetes MellitusEBioMedicine
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