Search results for "Type I"

showing 10 items of 966 documents

Estradiol, acting through estrogen receptor alpha, restores dimethylarginine dimethylaminohydrolase activity and nitric oxide production in oxLDL-tre…

2011

Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) synthase. ADMA accumulation, mainly due to a decreased dimethylarginine dimethylaminohydrolase (DDAH) activity, has been related to the development of cardiovascular diseases. We investigate whether estradiol prevents the changes induced by oxidized low density lipoprotein (oxLDL) on the DDAH/ADMA/NO pathway in human umbilical artery endothelial cells (HUAEC). HUAEC were exposed to estradiol, native LDL (nLDL), oxLDL and their combinations for 24 h. In some experiments, cells were also exposed to the unspecific estrogen receptor (ER) antagonist ICI 182780, the specific ERα antagonist MPP or specific agonists …

medicine.medical_specialtyProtein-Arginine N-MethyltransferasesEndotheliumNitric Oxide Synthase Type IIImedicine.drug_classBlotting WesternArginineNitric OxideBiochemistryUmbilical ArteriesNitric oxideAmidohydrolasesReceptors G-Protein-Coupledchemistry.chemical_compoundEndocrinologyEnosInternal medicinemedicineEstrogen Receptor betaHumansEstrogens Non-SteroidalMolecular BiologyCells CulturedbiologyEstradiolArtèriesProtein StabilityEstrogen AntagonistsEstrogen Receptor alphaEndoteli vascularbiology.organism_classificationNitric oxide synthaseIsoenzymesLipoproteins LDLRepressor Proteinsmedicine.anatomical_structureEndocrinologychemistryReceptors EstrogenEstrogenbiology.proteinlipids (amino acids peptides and proteins)Endothelium VascularAsymmetric dimethylarginineEstrogen receptor alphaGPER
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Biopterin metabolism and eNOS expression during hypoxic pulmonary hypertension in mice.

2013

International audience; Tetrahydrobiopterin (BH$_4$), which fosters the formation of and stabilizes endothelial NO synthase (eNOS) as an active dimer, tightly regulates eNOS coupling / uncoupling. Moreover, studies conducted in genetically-modified models demonstrate that BH$_4$ pulmonary deficiency is a key determinant in the pathogenesis of pulmonary hypertension. The present study thus investigates biopterin metabolism and eNOS expression, as well as the effect of sepiapterin (a precursor of BH$_4$) and eNOS gene deletion, in a mice model of hypoxic pulmonary hypertension. In lungs, chronic hypoxia increased BH$_4$ levels and eNOS expression, without modifying dihydrobiopterin (BH$_2$, t…

medicine.medical_specialtySepiapterinNitric Oxide Synthase Type III[SDV]Life Sciences [q-bio]Hypertension PulmonaryBiopterinlcsh:Medicine[SDV.BC]Life Sciences [q-bio]/Cellular Biology[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]030204 cardiovascular system & hematology03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineEnosRight ventricular hypertrophyDihydrobiopterinInternal medicinemedicine[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]AnimalsHypoxialcsh:Science[SDV.BC] Life Sciences [q-bio]/Cellular Biology030304 developmental biology0303 health sciencesMultidisciplinarybiologylcsh:RHypoxia (medical)biology.organism_classificationmedicine.diseasePulmonary hypertensionBiopterin[SDV] Life Sciences [q-bio]Disease Models AnimalTetrahydrofolate DehydrogenaseEndocrinologychemistryVentricular pressurelcsh:Qmedicine.symptomResearch ArticlePLoS ONE
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Prevention of Atherosclerosis by Interference with the Vascular Nitric Oxide System

2009

Nitric oxide (NO) produced by endothelial NO synthase (eNOS) represents an anti-atherosclerotic principle. NO bioavailability is decreased in atherosclerosis due to increased NO inactivation by reactive oxygen species and reduced NO synthesis. Various types of vascular pathophysiology are associated with oxidative stress, with NADPH oxidases as the major source of reactive oxygen species. These inactivate NO. Also, oxidative stress is likely to be the main cause for oxidation of the essential NOS cofactor, tetrahydrobiopterin (BH(4)). A lack of BH(4) leads to eNOS uncoupling (i.e., uncoupling of oxygen reduction from NO synthesis in eNOS). Based on these pathomechanisms, the therapeutic pot…

medicine.medical_specialtySepiapterinNitric Oxide Synthase Type IIImedicine.drug_classGTP cyclohydrolase INitric Oxidemedicine.disease_causeRenin inhibitorNitric oxidechemistry.chemical_compoundEnosInternal medicineDrug DiscoverymedicineAnimalsHumansHypolipidemic AgentsPharmacologybiologyArteriesTetrahydrobiopterinAtherosclerosisbiology.organism_classificationNitric oxide synthaseOxidative StressTreatment OutcomeEndocrinologychemistrybiology.proteinOxidative stressSignal Transductionmedicine.drugCurrent Pharmaceutical Design
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Current insights into the German lipoprotein apheresis standard: PCSK9-inhibitors, lipoprotein apheresis or both?

2017

Abstract According to current European guidelines, lipid lowering therapy for progressive cardiovascular disease including cardiovascular events has to be focused on a target level for LDL-C. In contrast for Lp(a) a threshold has to be defined with respect to the method of measurement. However, due to new lipid lowering drug developments like PCSK9-inhibitors (PCSK-9-I) a therapeutic algorithm for patients with severe hypercholesterolemia or isolated Lipoprotein(a)-hyperlipoproteinemia with progressive cardiovascular disease may be necessary to manage the use of PCSK9-I, lipoprotein apheresis (LA) or both. The therapeutic approach for patients with homozygous familial hypercholesterolemia i…

medicine.medical_specialtySerine Proteinase InhibitorsDiseaseFamilial hypercholesterolemia030204 cardiovascular system & hematologyRisk AssessmentHyperlipoproteinemia Type II03 medical and health sciencesTherapeutic approach0302 clinical medicineRisk FactorsInternal medicineGermanyInternal MedicinemedicineHumans030212 general & internal medicinePCSK9 Inhibitorsbiologybusiness.industryPCSK9Anticholesteremic AgentsPCSK9 InhibitorsGeneral MedicineLipoprotein(a)Cholesterol LDLmedicine.diseaseCombined Modality TherapyEndocrinologyTreatment OutcomeCardiovascular Diseasesbiology.proteinCardiologyBlood Component Removallipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicinebusinessLipoprotein apheresisBiomarkersLipoproteinLipoprotein(a)Atherosclerosis. Supplements
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Genetically determined hypercholesterolaemia results into premature leucocyte telomere length shortening and reduced haematopoietic precursors

2020

Abstract Aims Leucocyte telomere length (LTL) shortening is a marker of cellular senescence and associates with increased risk of cardiovascular disease (CVD). A number of cardiovascular risk factors affect LTL, but the correlation between elevated LDL cholesterol (LDL-C) and shorter LTL is debated: in small cohorts including subjects with a clinical diagnosis of familial hypercholesterolaemia (FH). We assessed the relationship between LDL-C and LTL in subjects with genetic familial hypercholesterolaemia (HeFH) compared to those with clinically diagnosed, but not genetically confirmed FH (CD-FH), and normocholesterolaemic subjects. Methods and results LTL was measured in mononuclear cells-d…

medicine.medical_specialtySettore MED/09 - Medicina InternaCellular ageingEpidemiologyHypercholesterolemiaCD34Cellular senescence030204 cardiovascular system & hematologyHyperlipoproteinemia Type II03 medical and health sciencesMice0302 clinical medicineInternal medicineLeukocytesMedicineAnimalsHumansProgenitor cellHaematopoiesi030304 developmental biologyLdl cholesterol0303 health sciencesbusiness.industryCholesterol LDLTelomere3. Good healthTelomereHaematopoiesisIncreased riskEndocrinologymedicine.anatomical_structureCHDTelomeresBone marrowCardiology and Cardiovascular MedicinebusinessFamilial hypercholesterolaemia
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Long-term efficacy of lipoprotein apheresis and lomitapide in the treatment of homozygous familial hypercholesterolemia (HoFH): a cross-national retr…

2021

Abstract Background Homozygous familial hypercholesterolemia (HoFH) is a rare life-threatening condition that represents a therapeutic challenge. The vast majority of HoFH patients fail to achieve LDL-C targets when treated with the standard protocol, which associates maximally tolerated dose of lipid-lowering medications with lipoprotein apheresis (LA). Lomitapide is an emerging therapy in HoFH, but its place in the treatment algorithm is disputed because a comparison of its long-term efficacy versus LA in reducing LDL-C burden is not available. We assessed changes in long-term LDL-C burden and goals achievement in two independent HoFH patients’ cohorts, one treated with lomitapide in Ita…

medicine.medical_specialtySettore MED/09 - Medicina Interna[SDV]Life Sciences [q-bio]LipoproteinsGenetic diseaseTherapeuticsFamilial hypercholesterolemiaDiseaseLipoprotein apheresiLDLHyperlipoproteinemia Type IIchemistry.chemical_compoundLipoprotein apheresisRetrospective surveyInternal medicineCholesterol burden; Genetic disease; Homozygous hypercholesterolemia; LDL; Lipoprotein apheresis; Lomitapide; Therapeutics; Benzimidazoles; Homozygote; Humans; Lipoproteins; Retrospective Studies; Anticholesteremic Agents; Blood Component Removal; Hyperlipoproteinemia Type IImedicineHumansPharmacology (medical)Genetics (clinical)Retrospective Studiesmedicine.diagnostic_testbusiness.industryResearchAnticholesteremic AgentsHomozygous hypercholesterolemiaHomozygoteRGeneral Medicinemedicine.diseaseLomitapideLomitapidecholesterol burden; genetic disease; homozygous hypercholesterolemia; LDL; lipoprotein apheresis; lomitapide; therapeuticsCholesterol burdenchemistryCohortBlood Component RemovalMedicineTherapeutics.BenzimidazolesLipid profilebusinessLipoprotein apheresisCross nationalOrphanet Journal of Rare Diseases
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Growth and differentiation factor 11 (GDF11): Functions in the regulation of erythropoiesis and cardiac regeneration

2015

International audience; Members of the TGF-β superfamily transduce their signals through type I and II receptor serine/threonine kinases. The binding of activins to activin type IIA (ActRIIA) or type IIB (ActRIIB) receptors induces the recruitment and phosphorylation of an activin type I receptor (ALK4 and/or ALK7), which then phosphorylates the Smad2 and Smad3 intracellular signaling proteins. The regulation of members of the TGF-β family is known to be complex, because many proteins able to bind the ligands and inhibit their activities have been identified. Growth and differentiation factor 11 (Gdf11) belongs to the TGF-β family. GDF11, like other members of the TGF-β superfamily, is prod…

medicine.medical_specialtySmad2 ProteinProtein Serine-Threonine Kinases030204 cardiovascular system & hematologyBiology03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicineTGF beta signaling pathway[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineHumansRegeneration[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPharmacology (medical)PhosphorylationCCL11Activin type 2 receptors030304 developmental biologyPharmacology0303 health sciencesR-SMADcardiac regenerationGrowth differentiation factorHeartActivins[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemCell biologyBMPR2Growth Differentiation FactorsEndocrinologyBone Morphogenetic ProteinsGDF11Smad2 ProteinSignal transductionActivin Receptors Type IerythropoiesisACVR2BSignal TransductionPharmacology & Therapeutics
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Effects of BIS076 in a model of osteoarthritis induced by anterior cruciate ligament transection in ovariectomised rats

2015

Background Osteoarthritis (OA) is the most frequent articular disease and a leading cause of disability. There is a need for effective treatments able to slow the progression of disease. Some of the available treatments are dietary supplements providing natural components. Recent studies have shown that estrogen deficiency contributes to the pathophysiological events of OA progression. Methods We have used the anterior cruciate ligament transection model of OA in ovariectomised rats to study the effects of BIS076, a new formulation of a natural porcine cartilage extract associated with hydroxyapatite (as a source of calcium) and vitamin D3. Cartilage degradation, proteoglycan depletion and …

medicine.medical_specialtySwineOvariectomyType II collagenOsteoarthritisCartilage Oligomeric Matrix ProteinBIS076DinoprostoneBone remodelingRheumatologyOsteoprotegerinInternal medicineOsteoarthritismedicineAnimalsOrthopedics and Sports MedicineRats WistarVitamin DCollagen Type IIGlycosaminoglycansBone mineralCartilage oligomeric matrix proteinbiologybusiness.industryTissue ExtractsCartilageAnterior Cruciate Ligament InjuriesArticular cartilage damageOsteoarthritis Kneemedicine.diseasePeptide FragmentsSurgeryRatsDisease Models Animalmedicine.anatomical_structureEndocrinologyDurapatiteTreatment Outcomebiology.proteinAnterior cruciate ligament transection modelCytokinesFemaleMatrix Metalloproteinase 3businessOvariectomised ratsBiomarkersResearch ArticleBMC Musculoskeletal Disorders
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Effect of CYP1A1 Gene Polymorphisms on Estrogen Metabolism and Bone Density

2004

UNLABELLED: In this study, we evaluated the effect of polymorphisms of the CYP1A1 gene, linked to hormone-related cancers, on estrogen metabolism and BMD. We found that variants carrying the A allele (CA and AA) for the C4887A polymorphism have a significantly higher degree of estrogen catabolism and lower femoral BMD. INTRODUCTION: Polymorphisms of the CYP1A1 gene, one of the key enzymes that metabolize estrogen, have been linked with hormone-related cancers. We investigated the impact of these polymorphisms on estrogen metabolism and BMD, which is another hormone-dependent health issue. MATERIALS AND METHODS: One hundred seventy postmenopausal women (mean age, 63.5 +/- 0.6 years) particip…

medicine.medical_specialtyTime FactorsGenotypeBone densitymedicine.drug_classEndocrinology Diabetes and MetabolismOsteoporosisRadioimmunoassayBiologyArticleCollagen Type IBone resorptionImmunoenzyme TechniquesAbsorptiometry PhotonBone DensityRisk FactorsInternal medicinehormones and receptorGenotypeCytochrome P-450 CYP1A1medicineHumansosteoporosiOrthopedics and Sports MedicineFemurBone ResorptionAllelesAgedPolymorphism GeneticEstradiolgenetic researchEstrogensMiddle Agedmedicine.diseaseGenotype frequencyPostmenopauseMenopauseEndocrinologyEstrogenepidemiologyFemaleCollagenGene polymorphismMenopausePeptidesPolymorphism Restriction Fragment LengthJournal of Bone and Mineral Research
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Diagnostic efficacy of the fluorometric determination of enzyme activity for Pompe disease from dried blood specimens compared with lymphocytes-possi…

2009

Pompe disease is a rare, autosomal-recessive disorder which results from a defect in the lysosomal enzyme acid alpha-glucosidase (GAA). The onset of this disease is highly variable, with infantile types being the most severe. Traditionally, lymphocytes, fibroblasts or muscle biopsies were necessary for enzyme activity measurement, because these materials do not express maltase-glucoamylase (MGA) that interferes with the assay. Recently, acarbose was found to inhibit MGA activity selectively, so that dried blood became accessible for GAA assessment.To evaluate the diagnostic efficacy of GAA measurement in dried blood specimens (DBSs) in comparison with lymphocytes. If DBSs provided reliable …

medicine.medical_specialtyTime FactorsLymphocyteBiopsyNeonatal ScreeningInternal medicineBiopsyGeneticsmedicineHumansFalse Positive ReactionsFluorometryLymphocytesGenetics (clinical)Acarbosechemistry.chemical_classificationNewborn screeningmedicine.diagnostic_testbiologybusiness.industryGlycogen Storage Disease Type IIMusclesInfant NewbornReproducibility of Resultsalpha-GlucosidasesEnzyme replacement therapyFibroblastsHydrogen-Ion ConcentrationEnzyme assaymedicine.anatomical_structureEndocrinologyEnzymechemistryCarbohydrate Metabolism Disorderbiology.proteinFeasibility Studiesbusinessmedicine.drugJournal of inherited metabolic disease
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