Search results for "apolipoproteins"

showing 10 items of 175 documents

Low birth weight at term impairs cord serum lipoprotein compositions and concentrations

1998

The purpose of this study was to determine the effect of low birth weight at term on serum lipoproteins. Lipid and apolipoprotein (apo) contents were investigated in cord sera of small-for-gestational-age (SGA) newborns at term (2290 g +/- 33 g) and compared with those of appropriate-for-gestational-age (AGA) newborns (3570 g +/- 93 g). In SGA newborns, VLDL amounts were twofold higher, whereas LDL, HDL2 and HDL3 contents were lower than in AGA newborns (-38%, -44% and -42%, respectively). VLDL-triacylglycerols (TG), apo B-100 and apo E were higher, while VLDL-apo C-II values were 39% lower in SGA newborns compared with those of AGA newborns. In SGA newborns, HDL2-apolipoprotein, phospholip…

MaleApolipoprotein EVery low-density lipoproteinmedicine.medical_specialtyApolipoprotein BLipoproteinsPhospholipidchemistry.chemical_compoundReference ValuesInternal medicineBlood plasmamedicineHumansreproductive and urinary physiologyFetal Growth Retardationbiologybusiness.industryInfant NewbornInfant Low Birth WeightFetal Bloodfemale genital diseases and pregnancy complicationsLow birth weightApolipoproteinsEndocrinologychemistryInfant Small for Gestational AgePediatrics Perinatology and Child Healthbiology.proteinCholesteryl esterFemalelipids (amino acids peptides and proteins)medicine.symptombusinessLipoproteinEuropean Journal of Pediatrics
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Apoe genotypes and brain imaging classes in normal cognition, mild cognitive impairment, and alzheimer’s disease: A longitudinal study

2020

Objective: To evaluate in 419 stroke-free cognitively normal subjects (CN) aged 45-82 years covering during a long prospective study (11.54 ± 1.47 years) the preclinical to dementia spectrum: 1) the distribution of small vessel disease (V) and brain atrophy (A) aggregated as following: V−/A−, V−/A+, V+/A−, V+/A+; 2) the relationship of these imaging classes with individual apolipoprotein E (APOE) genotypes; 3) the risk of progression to Alzheimer Disease (AD) of the individual APOE genotypes. Methods: Participants underwent one baseline (t0), and 4 clinical and neuropsychological assessments (t1,t2,t3, and t4). Brain MRI was performed in all subjects at t0, t2, t3 and t4.. White matter hyp…

MaleApolipoprotein Emedicine.medical_specialtyGenotypeApolipoprotein E4NeuroimagingNeuropsychological TestsAPOE genotypes Brain imaging classes Caudate atrophy Global cerebral atrophy Lacunes White matter hyperintensities Aged Aged 80 and over Alzheimer Disease Apolipoprotein E4 Apolipoproteins E Brain Case-Control Studies Cognitive Dysfunction Disease Progression Female Genotype Humans Longitudinal Studies Magnetic Resonance Imaging Male Middle Aged Neuroimaging Neuropsychological Tests Risk Factorsbrain imaging classesApolipoproteins EAtrophyNeuroimagingAlzheimer DiseaseRisk FactorsInternal medicineGlobal brain atrophymedicineHumansDementiaCognitive DysfunctionLongitudinal Studiescaudate atrophyAgedglobal cerebral atrophyAged 80 and overAPOE genotypesbusiness.industryNeuropsychologyBrainMiddle Agedwhite matter hyperintensitiesmedicine.diseaseMagnetic Resonance ImagingHyperintensityNeurologyCase-Control StudiesDisease ProgressionCardiologyFemaleNeurology (clinical)Alzheimer's diseasebusiness
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Apolipoprotein E isoforms and the development of low and high Braak stages of Alzheimer's disease-related lesions

1999

In recent research, apolipoprotein-E (apoE) polymorphism has been shown to influence the formation of neurofibrillary changes and the accumulation of beta/A4-amyloid, the histopathological hallmarks of Alzheimer's disease (AD). Clinical studies associate the apoE allele epsilon4 with earlier onset of the disease, although the clinical speed of progression remains unchanged. Time course estimates have also provided evidence which indicates that the clinical phase of AD constitutes only 10-20% of the total time span needed for the development of this slowly progressing degenerative brain disorder. Due to the lack of reliable clinical tests for the detection of pre-symptomatic stages of AD, we…

MaleApolipoprotein Emedicine.medical_specialtyPathologyGenotypeApolipoprotein BApolipoprotein E2Apolipoprotein E4Apolipoprotein E3tau ProteinsNeuropathologyPathology and Forensic MedicineCellular and Molecular NeuroscienceApolipoproteins EDegenerative diseaseIsomerismAlzheimer DiseaseInternal medicineGenotypemedicineHumansAlleleAllelesBrain ChemistryAmyloid beta-PeptidesPolymorphism GeneticbiologyBrainNeurofibrillary TanglesNeurofibrillary tangleMiddle Agedmedicine.diseaseEndocrinologyDisease Progressionbiology.proteinFemaleNeurology (clinical)Alzheimer's diseaseActa Neuropathologica
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Midostaurin upregulates eNOS gene expression and preserves eNOS function in the microcirculation of the mouse

2005

Nitric oxide (NO) derived from endothelial NO synthase (eNOS) is a powerful vasodilator and possesses vasoprotective effects. Therefore, augmentation of eNOS expression and -activity by pharmacological means could provide protection against cardiovascular disease. However, this concept has been questioned recently, because in several disease models, eNOS upregulation was associated with a dysfunctional enzyme (referred to as eNOS uncoupling). In contrast, the present study demonstrates that an eNOS gene expression-enhancing compound with additional protein kinase C (PKC) inhibitory properties can upregulate eNOS while preserving its enzymatic function. Apolipoprotein E-knockout mice were tr…

MaleCancer ResearchNitric Oxide Synthase Type IIIPhysiologyClinical BiochemistryNitric Oxide Synthase Type IIBiologyPharmacologyBiochemistryNitric oxideMicechemistry.chemical_compoundApolipoproteins EEnosmedicineAnimalsStaurosporineRNA MessengerMidostaurinAortaNitritesProtein kinase CMice KnockoutNitratesMicrocirculationStaurosporinebiology.organism_classificationVasoprotectiveVasodilationNitric oxide synthaseBiochemistrychemistryEnzyme Inductionbiology.proteinNitric Oxide SynthaseReactive Oxygen SpeciesIntravital microscopymedicine.drugNitric Oxide
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Molecular diagnosis of hypobetalipoproteinemia: an ENID review.

2007

Abstract Primary hypobetalipoproteinemia (HBL) includes a group of genetic disorders: abetalipoproteinemia (ABL) and chylomicron retention disease (CRD), with a recessive transmission, and familial hypobetalipoproteinemia (FHBL) with a co-dominant transmission. ABL and CRD are rare disorders due to mutations in the MTP and SARA2 genes, respectively. Heterozygous FHBL is much more frequent. FHBL subjects often have fatty liver and, less frequently, intestinal fat malabsorption. FHBL may be linked or not to the APOB gene. Most mutations in APOB gene cause the formation of truncated forms of apoB which may or may be not secreted into the plasma. Truncated apoBs with a size below that of apoB-3…

MaleCandidate geneSettore MED/09 - Medicina InternaApolipoprotein BGenotypeLocus (genetics)BiologyPolymorphism Single NucleotidePCSK9 GenemedicineHumansFamilial hypobetalipoproteinemiaGenetic TestingAPOB geneApolipoproteins BGeneticsPCSK9AbetalipoproteinemiaChylomicron retention diseasemedicine.diseaseEuropean Network for Inherited Dyslipidemia (ENID)AbetalipoproteinemiaPhenotypePCSK9 geneHypobetalipoproteinemia Familial Apolipoprotein BMutationbiology.proteinlipids (amino acids peptides and proteins)FemaleHypobetalipoproteinemiaMTP geneCardiology and Cardiovascular MedicineCarrier Proteinsuropean Network for Inherited Dyslipidemia (ENID)European Network for Inherited Dyslipidemia (ENID) Familial hypobetalipoproteinemia Abetalipoproteinemia Chylomicron retention disease.Chylomicron retention diseaseAtherosclerosis
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Towards early risk biomarkers: serum metabolic signature in childhood predicts cardio-metabolic risk in adulthood

2021

Summary: Background: Cardiovascular diseases may originate in childhood. Biomarkers identifying individuals with increased risk for disease are needed to support early detection and to optimise prevention strategies. Methods: In this prospective study, by applying a machine learning to high throughput NMR-based metabolomics data, we identified circulating childhood metabolic predictors of adult cardiovascular disease risk (MetS score) in a cohort of 396 females, followed from childhood (mean age 11·2 years) to early adulthood (mean age 18·1 years). The results obtained from the discovery cohort were validated in a large longitudinal birth cohort of females and males followed from puberty to…

MaleGerontologyMedicine (General)Longitudinal studyApolipoprotein BbiomarkkeritDiseaseType 2 diabetesRisk FactorsInformed consentProspective StudiesChildProspective cohort studyFinlandmedia_commonFramingham Risk ScorebiologyRriskitekijätGeneral MedicineALSPACmetabolomicsaikuisuusCardiovascular DiseasesCohortMedicineBirth CohortFemaleResearch Papermedicine.medical_specialtyAdolescentlongitudinal-studypitkittäistutkimusGeneral Biochemistry Genetics and Molecular BiologyR5-920childrencardio-metabolic riskInternal medicinemedicineHumansmedia_common.cataloged_instanceEuropean unionApolipoproteins AApolipoproteins Bbusiness.industryPubertyCardio metabolic risklapsuusmedicine.diseaseCross-Sectional StudiesDiabetes Mellitus Type 2biology.proteinsydän- ja verisuonitauditaineenvaihduntatuotteetbusinessBiomarkersDeclaration of HelsinkieBioMedicine
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Effect of hypolipidemic treatment on emerging risk factors in mixed dyslipidemia: a randomized pilot trial

2012

Background The effects of different hypolipidemic treatment strategies on emerging atherosclerosis risk factors remain unknown. Materials and methods This is a prespecified analysis of a prospective, randomized, open-label, blinded end point (PROBE) study (ClinicalTrials.gov identifier: NCT01010516). Patients (n = 100) with mixed dyslipidaemia on a standard statin dose who had not achieved lipid targets were randomized to switch to the highest dose of rosuvastatin (40 mg/day) or to add-on-statin extended release nicotinic acid (ER-NA)/laropiprant (LRPT) or to add-on-statin micronized fenofibrate for a total of 3 months. Results Following 3 months of treatment, low-density lipoprotein (LDL) …

MaleIndolesTime FactorsClinical BiochemistryPilot ProjectsPharmacologyBiochemistryGastroenterologychemistry.chemical_compoundFenofibrateRisk FactorsProspective StudiesRosuvastatin CalciumHypolipidemic AgentsSulfonamidesFenofibratebiologyGeneral MedicineMiddle AgedRosuvastatin CalciumC-Reactive ProteinCardiovascular DiseasesDrug Therapy CombinationFemalelipids (amino acids peptides and proteins)Laropiprantmedicine.drugAdultmedicine.medical_specialtyStatinmedicine.drug_classNiacinInternal medicinemedicineHumansRosuvastatinAgedApolipoproteins BDyslipidemiasbusiness.industryCholesterolC-reactive proteinnutritional and metabolic diseasesCholesterol LDLAtherosclerosismedicine.diseaseFluorobenzenesPyrimidineschemistry1-Alkyl-2-acetylglycerophosphocholine Esterasebiology.proteinHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessDyslipidemiaEuropean Journal of Clinical Investigation
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Antiatherosclerotic Effects of Small-Molecular-Weight Compounds Enhancing Endothelial Nitric-Oxide Synthase (eNOS) Expression and Preventing eNOS Unc…

2008

Many cardiovascular diseases are associated with reduced levels of bioactive nitric oxide (NO) and an uncoupling of oxygen reduction from NO synthesis in endothelial NO synthase (eNOS uncoupling). In human endothelial EA.hy 926 cells, two small-molecular-weight compounds with related structures, 4-fluoro-N-indan-2-yl-benzamide (CAS no. 291756-32-6; empirical formula C16H14FNO; AVE9488) and 2,2-difluoro-benzo[1,3]dioxole-5-carboxylic acid indan-2-ylamide (CAS no. 450348-85-3; empirical formula C17H13F2NO3; AVE3085), enhanced eNOS promoter activity in a concentration-dependent manner; with the responsible cis-element localized within the proximal 263 base pairs of the promoter region. RNA int…

MaleNeointimamedicine.medical_specialtyNitric Oxide Synthase Type IIINitric Oxide Synthase Type IINitric OxideProtective AgentsUmbilical veinCell LineNitric oxideMicechemistry.chemical_compoundApolipoproteins EEnosInternal medicinemedicineAnimalsHumansBenzodioxolesRNA MessengerAortaMice KnockoutPharmacologychemistry.chemical_classificationSp1 transcription factorReactive oxygen speciesGene knockdownbiologyEndothelial CellsAtherosclerosisbiology.organism_classificationVasoprotectiveMice Inbred C57BLMolecular WeightEndocrinologychemistryBenzamidesIndansMolecular MedicineJournal of Pharmacology and Experimental Therapeutics
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Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX 3 CL1) Expression by Angiotensin-II

2012

Objective— Angiotensin-II (Ang-II) promotes the interaction of mononuclear cells with arterioles and neutrophils with postcapillary venules. To investigate the mechanisms underlying this dissimilar response, the involvement of fractalkine (CX 3 CL1) was explored. Methods and Results— Enhanced CX 3 CL1 expression was detected in both cremasteric arterioles and postcapillary venules 24 hours after Ang-II intrascrotal injection. Arteriolar leukocyte adhesion was the unique parameter significantly reduced (83%) in animals lacking CX 3 CL1 receptor (CX 3 CR1). Human umbilical arterial and venous endothelial cell stimulation with 1 μmol/L Ang-II increased CX 3 CL1 expression, yet neutralization …

MalePathologyTime Factorsp38 Mitogen-Activated Protein KinasesMiceVenulesLeukocytesEndothelial dysfunctionExtracellular Signal-Regulated MAP KinasesReceptorCells CulturedMice KnockoutMembrane GlycoproteinsAngiotensin IINF-kappa BArteriesEndothelial stem cellArteriolesNADPH Oxidase 5NADPH Oxidase 4NADPH Oxidase 2FemaleRNA InterferenceReceptors ChemokineTumor necrosis factor alphaCardiology and Cardiovascular MedicineSignal Transductionmedicine.medical_specialtyCX3C Chemokine Receptor 1BiologyTransfectionPeripheral blood mononuclear cellLosartanVeinsInterferon-gammaApolipoproteins EDownregulation and upregulationInternal medicineCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansLeukocyte RollingCX3CL1Chemokine CX3CL1Tumor Necrosis Factor-alphaEndothelial CellsMembrane ProteinsNADPH OxidasesAtherosclerosismedicine.diseaseAngiotensin IIMice Inbred C57BLDisease Models AnimalEndocrinologyAngiotensin II Type 1 Receptor BlockersArteriosclerosis, Thrombosis, and Vascular Biology
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Limited agreement between biomarkers of neuronal injury at different stages of Alzheimer's disease

2013

Abstract New diagnostic criteria for Alzheimer's disease (AD) treat different biomarkers of neuronal injury as equivalent. Here, we quantified the degree of agreement between hippocampal volume on structural magnetic resonance imaging, regional glucose metabolism on positron emission tomography, and levels of phosphorylated tau in cerebrospinal fluid (CSF) in 585 subjects from all phases of the AD Neuroimaging Initiative. The overall chance-corrected agreement was poor (Cohen κ, 0.24–0.34), in accord with a high rate of conflicting findings (26%–41%). Neither diagnosis nor APOE e4 status significantly influenced the distribution of agreement between the biomarkers. The degree of agreement t…

MalePathologymedicine.medical_specialtyEpidemiologytau ProteinsHippocampus03 medical and health sciencesCellular and Molecular NeuroscienceApolipoproteins E0302 clinical medicineAtrophyCerebrospinal fluidDevelopmental NeuroscienceNeuroimagingAlzheimer DiseaseFluorodeoxyglucose F18medicineHumansDementiaCognitive DysfunctionAged030304 developmental biology0303 health sciencesChi-Square Distributionmedicine.diagnostic_testHealth PolicyMiddle Agedmedicine.diseasePsychiatry and Mental healthPositron emission tomographyPositron-Emission TomographyBiomarker (medicine)FemaleNeurology (clinical)AtrophyGeriatrics and GerontologyAlzheimer's diseaseMental Status SchedulePsychologyChi-squared distributionBiomarkers030217 neurology & neurosurgeryAlzheimer's & Dementia
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