Search results for "Apolipoprotein"

showing 10 items of 354 documents

Systematic review by meta-analyses on the possible role of TNF-alpha polymorphisms in association with Alzheimer's disease.

2009

It has been hypothesized that polymorphisms of Tumor Necrosis Factor (TNF)-alpha gene affect the risk of developing Alzheimer's disease (AD). However, results of different studies are often inconsistent. Our aim was to investigate by meta-analysis the association of the common polymorphisms comprehensively defining the genetic variability of the TNF-alpha gene with AD risk. Hence, the results being stated are of a meta-analysis across studies, and that this meta-analysis does not invalidate the results of the individual studies previously performed. Seventeen studies that investigated the association between 5 TNF-alpha polymorphisms (-850, -308, -863, -238, and -1031) and AD were retrieved…

Settore MED/04 - Patologia GeneraleOncologyApolipoprotein Emedicine.medical_specialtybusiness.industryTumor Necrosis Factor-alphaGeneral NeuroscienceOdds ratioPolymorphism Single NucleotideALZHEIMER'S DISEASE CYTOKINESDEMENTIAGENETICSMETA-ANALYSISPOLYMORPHISM TUMOR NECROSIS FACTORPolymorphism (computer science)Alzheimer DiseaseInternal medicineMeta-analysisGenotypeImmunologymedicineOdds RatioSettore MED/05 - Patologia ClinicaHumansNeurology (clinical)Genetic variabilityAllelebusinessGenetic associationBrain research reviews
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Lipid and apoprotein composition of HDL in partial or complete CETP deficiency

2012

Hyperalphalipoproteinemia, as observed in patients who are either homozygous or heterozygous for cholesteryl ester transfer protein (CETP) deficiency, has been shown to be associated with striking changes in apolipoprotein size distribution, namely, of high-density lipoprotein (HDL) and HDL-like particles. We compared the effect of varying degrees of CETP activity on the HDL apolipoprotein profile in Caucasian CETP-deficient subjects and following pharmacological decrease in CETP activity, using Size Exclusion Chromatography followed by Reverse Phase Protein Array (SEC RPA). The main HDL-associated apolipoproteins (Apo), i.e. ApoA-I, ApoA-II, ApoC-I, and ApoC-III, co-eluted with the HDL pea…

Settore MED/09 - Medicina InternaApolipoprotein BCholesterol Ester Transfer Proteinmedicine.disease_causereverse phase protein arraychemistry.chemical_compoundExonMutationbiologyHomozygotescavenger receptor class B1size exclusion chromatographyLipidCholesteryl ester transfer proteinLipidstorcetrapibApolipoproteinBiochemistryELISAlipids (amino acids peptides and proteins)hyperalphalipoproteinemiaCardiology and Cardiovascular MedicineLipoproteins HDLHumandalcetrapibmedicine.medical_specialtyHeterozygoteDalcetrapibHypercholesterolemiaapolipoproteinhigh-density lipoproteinInternal medicineCholesterylester transfer proteinmedicineAnimalsHumansCholesteryl ester transfer protein; dalcetrapib; high-density lipoprotein; reverse phase protein array; scavenger receptor class B1; size exclusion chromatography; torcetrapib; apolipoprotein; hyperalphalipoproteinemia; ELISAPharmacologybusiness.industryAnimalPoint mutationCholesterol HDLTorcetrapibnutritional and metabolic diseasesLipid MetabolismCholesterol Ester Transfer Proteinscarbohydrates (lipids)Disease Models AnimalEndocrinologyApolipoproteinschemistrybiology.proteinbusinessLipoprotein
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eNOS Activation by HDL Is Impaired in Genetic CETP Deficiency.

2014

Mutations in the CETP gene resulting in defective CETP activity have been shown to cause remarkable elevations of plasma HDL-C levels, with the accumulation in plasma of large, buoyant HDL particles enriched in apolipoprotein E. Genetic CETP deficiency thus represents a unique tool to evaluate how structural alterations of HDL impact on HDL atheroprotective functions. Aim of the present study was to assess the ability of HDL obtained from CETP-deficient subjects to protect endothelial cells from the development of endothelial dysfunction. HDL isolated from one homozygous and seven heterozygous carriers of CETP null mutations were evaluated for their ability to down-regulate cytokine-induced…

Settore MED/09 - Medicina InternaCHOLESTEROL EFFLUXApolipoprotein BEpidemiologylcsh:MedicineANTIINFLAMMATORY PROPERTIESmedicine.disease_causeBiochemistryVascular Medicinechemistry.chemical_compoundHigh-density lipoproteinEnosMedicine and Health SciencesEndothelial dysfunctionlcsh:ScienceMutationMultidisciplinarybiologyHomozygoteCETP; eNOS; HDL;NeurochemistryLipidsGenetic EpidemiologyeNOSlipids (amino acids peptides and proteins)AnatomyNeurochemicalsLipoproteins HDLResearch Articlemedicine.medical_specialtyDrug Research and DevelopmentHDLNitric Oxide Synthase Type IIILipoproteinsENDOTHELIAL FUNCTIONINHIBITIONCardiologyDown-RegulationVascular Cell Adhesion Molecule-1Nitric OxideCELL-ADHESION MOLECULE-1Lipid Metabolism Inborn ErrorsESTER TRANSFER PROTEINInternal medicineCETPCholesterylester transfer proteinHuman Umbilical Vein Endothelial CellsmedicineHumansNITRIC-OXIDE SYNTHASEInflammationClinical GeneticsPharmacologyCholesterollcsh:RTorcetrapibEndothelial CellsBiology and Life SciencesProteinsnutritional and metabolic diseasesLipid MetabolismAtherosclerosismedicine.diseasebiology.organism_classificationCholesterol Ester Transfer Proteinscarbohydrates (lipids)MetabolismEndocrinologychemistryOther Clinical MedicineMutationImmunologyCardiovascular Anatomybiology.proteinlcsh:QTORCETRAPIBClinical MedicineHIGH-DENSITY-LIPOPROTEINSCAVENGER RECEPTOR BI
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Hypobetalipoproteinemia: genetics, biochemistry, and clinical spectrum.

2011

Hypobetalipoproteinemias (HBL) represent a heterogeneous group of disorders characterized by reduced plasma levels of total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C) and apolipoprotein B (apoB) below the 5th percentile of the distribution in the population. HBL are defined as primary or secondary according to the underlying causes. Primary monogenic HBL are caused by mutations in several known genes (APOB, PCSK9, MTP, SARA2) or mutations in genes not yet identified. Familial hypobetalipoproteinemia (FHBL) is the most frequent monogenic form of HBL with a dominant mode of inheritance. It may be due to loss-of-function mutations in APOB or, less frequently, in PCSK9 genes.…

Settore MED/09 - Medicina InternaPrimary hypobetalipoproteinemiasrecessive formsdominant formsclinical phenotypediagnostic algorithmHypobetalipoproteinemiasLiverReceptors LDLPrimary hypobetalipoproteinemias; dominant forms; recessive forms; clinical phenotype; secondary hypobetalipoproteinemias; diagnostic algorithm.secondary hypobetalipoproteinemiasHumansHypobetalipoproteinemiaApolipoproteins B
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Apolipoprotein A1 in Cerebrospinal Fluid Is Insufficient to Distinguish Alzheimer's Disease from Other Dementias in a Naturalistic, Clinical Setting.

2020

Apolipoprotein A1 (ApoA1) is the major protein component of the high-density lipoprotein and involved in cholesterol transport. Disruption of cholesterol homeostasis has been identified as a contributing factor for Alzheimer's disease (AD). Moreover, polymorphisms of ApoA1 have been associated with higher risk of disease onset and cognitive decline. Therefore, ApoA1 has been suggested as a biomarker in AD. Here, we tested a small cohort of AD and non-AD dementia patients and measured levels of ApoA1 in cerebrospinal fluid. Our results indicate that ApoA1 might not be applicable to distinguish AD from other forms of dementia.

Short CommunicationDiseasecerebrospinal fluidchemistry.chemical_compoundmedicineDementiaCognitive declinebiologyCholesterolbusiness.industryGeneral Neurosciencemedicine.diseasePsychiatry and Mental healthClinical PsychologychemistryCohortImmunologybiology.proteinBiomarker (medicine)biomarkerApolipoprotein A1lipids (amino acids peptides and proteins)Apolipoprotein A1Geriatrics and GerontologybusinessAlzheimer’s diseaseLipoproteindementiaJournal of Alzheimer's disease reports
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Tribolium castaneum immune defense genes are differentially expressed in response to Bacillus thuringiensis toxins sharing common receptor molecules …

2015

In Tribolium castaneum larvae we have demonstrated by RNA interference knockdown that the Bacillus thuringiensis Cry3Ba toxin receptors Cadherin-like and Sodium solute symporter proteins are also functional receptors of the less active Cry3Aa toxin. Differences in susceptibility to B. thuringiensis infection might not only rely on toxin-receptor interaction but also on host defense mechanisms. We compared the expression of the immune related genes encoding Apolipophorin-III and two antimicrobial peptides, Defensin3 and Defensin2 after B. thuringiensis challenge. All three genes were up-regulated following Cry3Ba spore-crystal intoxication whereas only Defensins gene expression was induced u…

Staphylococcus aureusImmunologyAntimicrobial peptidesBacterial ToxinsMolecular Sequence DataBacillus thuringiensisBiologymedicine.disease_causeMicrobiologyDefensinsHemolysin ProteinsImmune systemBacterial ProteinsRNA interferenceBacillus thuringiensisGene expressionCandida albicansmedicineEscherichia coliAnimalsAmino Acid SequenceRNA Small InterferingDefensinTriboliumInnate immune systemBacillus thuringiensis ToxinsSymportersToxinfungibiology.organism_classificationAnti-Bacterial AgentsEndotoxinsApolipoproteinsLarvaInsect ProteinsRNA InterferenceDevelopmental BiologyDevelopmental and comparative immunology
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Lipid-Altering Efficacy of Ezetimibe/Simvastatin 10/20 mg Compared to Rosuvastatin 10 mg in High-Risk Patients with and without Type 2 Diabetes Melli…

2010

AIMS: This post hoc analysis compared the effects of switching to ezetimibe/simvastatin 10/20 mg (EZE/SIMVA) or rosuvastatin 10 mg (ROSUVA) in uncontrolled high-risk hypercholesterolemic patients with/without type 2 diabetes mellitus (T2DM) despite statin monotherapy. METHODS: Patients (n = 618) at high risk for coronary vascular disease with elevated LDL-C ≥100 and ≤190 mg/dL despite use of statins were randomized 1:1 to double-blind EZE/SIMVA 10/20 mg or ROSUVA 10 mg for 6 weeks. Patients were classified as having T2DM based on ≥1 of the following: diagnosis of T2DM, antidiabetic medication, or FPG ≥126 mg/dL. This analysis evaluated percent changes from baseline in lipids among patients …

SulfonamidesSimvastatinSettore MED/09 - Medicina InternaAnticholesteremic AgentsHypercholesterolemiaDrug ResistanceCholesterol LDLEzetimibeLipidsFluorobenzenesC-Reactive ProteinCholesterolPyrimidinesDiabetes Mellitus Type 2Double-Blind MethodOdds RatioDiabetes MellitusAzetidinesHumansDrug Therapy CombinationHydroxymethylglutaryl-CoA Reductase InhibitorsRosuvastatin CalciumApolipoproteins B
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New Lipid Modulating Drugs: The Role of Microsomal Transport Protein Inhibitors

2011

Microsomal triglyceride transfer protein (MTP) is involved in the synthesis of very low density lipoprotein in the liver. Its deficiency results in abetalipoproteinemia. MTP inhibitors target the assembly and secretion of apolipoprotein B-containing lipoproteins. These agents may potentially play a role, alone or in combination, in the treatment of hypercholesterolemia or hypertriglyceridemia. Clinical applications of MTP inhibitors initially focused primarily on high-dose monotherapy in order to produce substantial reductions in LDL-cholesterol levels but these proved to induce significant hepatic steatosis and transaminase elevations. However, likely orphan indications for MTP inhibitors,…

Very low-density lipoproteinApolipoprotein BHypercholesterolemiaFamilial hypercholesterolemiaLipoproteins VLDLPharmacologyMicrosomal triglyceride transfer proteinHyperlipoproteinemia Type IIchemistry.chemical_compoundMicrosomesDrug DiscoveryClinical endpointHumansMedicineApolipoproteins BHypertriglyceridemiaPharmacologybiologybusiness.industryCholesterolAbetalipoproteinemiamedicine.diseaseAbetalipoproteinemiaBiochemistrychemistryMTP-inhibitors lipids lipoproteins atherosclerosis cardiovascular prevention.biology.proteinlipids (amino acids peptides and proteins)SteatosisCarrier ProteinsbusinessCurrent Pharmaceutical Design
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Anti-inflammatory Function of High-Density Lipoproteins via Autophagy of IκB Kinase

2015

Background & Aims: Plasma levels of high-density lipoprotein (HDL) cholesterol are frequently found decreased in patients with inflammatory bowel disease (IBD). Therefore, and because HDL exerts anti-inflammatory activities, we investigated whether HDL and its major protein component apolipoprotein A-I (apoA-I) modulate mucosal inflammatory responses in vitro and in vivo. Methods: The human intestinal epithelial cell line T84 was used as the in vitro model for measuring the effects of HDL on the expression and secretion of tumor necrosis factor (TNF), interleukin-8 (IL-8), and intracellular adhesion molecule (ICAM). Nuclear factor-κB (NF-κB)-responsive promoter activity was studied by …

WT wild typeApolipoprotein BEMSA electrophoretic mobility shift assayMPO myeloperoxidaseIκB kinaseDSS dextran sodium sulphatemTOR the mammalian target of rapamycinRT-PCR real-time polymerase chain reactionNF-κBchemistry.chemical_compound540 ChemistryApoA-I apolipoprotein A-I10038 Institute of Clinical ChemistryOriginal ResearchTNF tumor necrosis factorbiologyIBD inflammatory bowel diseaseChemistryGastroenterologyMyeloperoxidase10076 Center for Integrative Human PhysiologyMEICS murine endoscopic index of colitis severityTumor necrosis factor alphalipids (amino acids peptides and proteins)3-MA 3-methyl adenineNF-κB nuclear factor κBHDL high-density lipoproteinLC3II light chain 3 IIPBS phosphate-buffered salinep-IKK phosphorylated IκB kinase610 Medicine & healthICAM intracellular adhesion molecule246-Trinitrobenzenesulfonic acidTg transgenicmedicineAutophagyCD Crohn’s disease2715 GastroenterologyColitislcsh:RC799-869KO knockoutHepatologyApolipoprotein A-IAutophagyInflammatory Bowel DiseaseTNBS 246-trinitrobenzenesulfonic acidmedicine.diseaseMolecular biologyIL interleukinsiRNA small interfering RNAPI-3 phosphatidylinositol-3Immunologybiology.protein2721 Hepatologylcsh:Diseases of the digestive system. GastroenterologyPFA paraformaldehydeLipoproteinDAPI 4′6-diamidino-2-phenylindoleCMGH Cellular and Molecular Gastroenterology and Hepatology
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Estudio del defecto familiar de unión de la apolipoproteína B100 en una población mediterránea

2004

Fundamento y objetivo Comparar las caracteristicas clinicobioquimicas del defecto familiar de union de la apolipoproteina B100 (DFB) con la hipercolesterolemia familiar (HF) heterocigota en una poblacion mediterranea del sur de Europa donde existen pocos datos al respecto, estudiar la prevalencia y el posible efecto fundador del DFB en una zona de la Comunidad Valenciana y conocer las caracteristicas clinicobioquimicas del DFB. Sujetos y metodo Hemos estudiado a 19 heterocigotos con DFB (8 varones) pertenecientes a 12 familias, portadores de la mutacion R3500Q del gen de la apolipoproteina B, y a 57 heterocigotos con HF (24 varones) geneticamente caracterizados, seleccionados de forma aleat…

business.industryMedicineGeneral MedicineApolipoproteins bbusinessHumanitiesMedicina Clínica
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