Search results for "statin"

showing 10 items of 545 documents

Familial hypercholesterolæmia in children and adolescents: Gaining decades of life by optimizing detection and treatment

2015

Contains fulltext : 155263.pdf (Publisher’s version ) (Open Access) Familial hypercholesterolaemia (FH) is a common genetic cause of premature coronary heart disease (CHD). Globally, one baby is born with FH every minute. If diagnosed and treated early in childhood, individuals with FH can have normal life expectancy. This consensus paper aims to improve awareness of the need for early detection and management of FH children. Familial hypercholesterolaemia is diagnosed either on phenotypic criteria, i.e. an elevated low-density lipoprotein cholesterol (LDL-C) level plus a family history of elevated LDL-C, premature coronary artery disease and/or genetic diagnosis, or positive genetic testin…

CounselingEuropean Atherosclerosis Society Consensus PanelPediatricsCardiac & Cardiovascular SystemsSTATIN THERAPYSettore MED/09 - Medicina InternaVascular damage Radboud Institute for Health Sciences [Radboudumc 16]Familial hypercholesterolemiaAdolescentsCarotid Intima-Media ThicknessINTIMA-MEDIA THICKNESSCost of IllnessPregnancyRisk FactorsDiagnosisYOUNG-ADULTSHIPERCOLESTEROLEMIA (DIAGNÓSTICO;TERAPIA;TENDÊNCIAS)Family historyYoung adultChildChildrenEvidence-Based Medicinemedicine.diagnostic_testHomozygoteMiddle AgedFamilial hypercholesterolæmia3. Good healthEconomics MedicalAdolescents; Children; Consensus statement; Diagnosis; Ezetimibe; Familial hypercholesterolæmia; LDL cholesterol; PCSK9 inhibitor; Statin; Treatment; Cardiology and Cardiovascular MedicineCARDIOVASCULAR-DISEASEConsensus statementLDL cholesterolFemalelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineFamilial hypercholesterolaemiaLife Sciences & BiomedicineDiagnosimedicine.drugAdultHeterozygotemedicine.medical_specialtyStatinAdolescentmedicine.drug_classPCSK9 inhibitorENDOTHELIAL FUNCTIONLOW-DENSITY-LIPOPROTEINReviewsCOST-EFFECTIVENESS ANALYSIS1102 Cardiovascular Medicine And HaematologyMedication AdherenceHyperlipoproteinemia Type IIYoung AdultLife ExpectancyEzetimibemedicineHumansCORONARY-HEART-DISEASEGenetic TestingGenetic testingPregnancyScience & TechnologyClinical Laboratory Techniquesbusiness.industryPreventionStatinAtherosclerosismedicine.diseaseEzetimibeDietASSOCIATION EXPERT PANELBLOOD-PRESSURE RESEARCHPregnancy ComplicationsTreatmentEarly DiagnosisIntima-media thicknessCardiovascular System & HematologyDietary SupplementsPhysical therapyCardiovascular System & Cardiologybusiness
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8.2 Glomerular Filtration Rate by Creatinine and Cystatin C Measurements in Essential Hypertensive Patients

2008

Creatininemedicine.medical_specialtybiologybusiness.industryUrologyRenal functionchemistry.chemical_compoundPharmacotherapychemistryCystatin CInternal Medicinebiology.proteinMedicineCardiology and Cardiovascular MedicinebusinessHigh Blood Pressure & Cardiovascular Prevention
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Lovastatin causes sensitization of HeLa cells to ionizing radiation‐induced apoptosis by the abrogation of G2 blockage

2003

To investigate the effect of inhibition of Ras/Rho-regulated signalling by 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) on radiation-induced cell killing and apoptosis.Different human cell lines were pretreated or not with lovastatin before exposure to gamma-rays. Afterwards, radiation-induced cell killing, formation and repair of double-strand breaks, activation of radiation-inducible signal mechanisms (i.e. p53, p21, extracellular-signal-related kinase (ERK), NF-kappaB), changes in cell cycle progression and apoptosis were analysed.As shown by a colony formation assay, lovastatin sensitized HeLa cells to gamma-radiation-induced cell killing. The lovastati…

Cyclin-Dependent Kinase Inhibitor p21G2 PhaseMAPK/ERK pathwayApoptosisBiologyHeLaCyclinspolycyclic compoundsmedicineHumansRadiology Nuclear Medicine and imagingLovastatinSensitizationRadiological and Ultrasound TechnologyKinaseNF-kappa Bnutritional and metabolic diseasesCell cyclebiology.organism_classificationCell biologyCell killingmedicine.anatomical_structureGamma RaysApoptosislipids (amino acids peptides and proteins)LovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsMitogen-Activated Protein KinasesTumor Suppressor Protein p53DNA DamageHeLa Cellsmedicine.drugInternational Journal of Radiation Biology
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Transcription of genes in the biosynthetic pathway for fumonisin mycotoxins is epigenetically and differentially regulated in the fungal maize pathog…

2012

ABSTRACT When the fungal pathogen Gibberella moniliformis (anamorph, Fusarium verticillioides ) colonizes maize and maize-based products, it produces class B fumonisin (FB) mycotoxins, which are a significant threat to human and animal health. FB biosynthetic enzymes and accessory proteins are encoded by a set of clustered and cotranscribed genes collectively named FUM, whose molecular regulation is beginning to be unraveled by researchers. FB accumulation correlates with the amount of transcripts from the key FUM genes, FUM1 , FUM21 , and FUM8 . In fungi in general, gene expression is often partially controlled at the chromatin level in secondary metabolism; when this is the case, the deac…

DISRUPTIONTranscription GeneticFUM21[SDV]Life Sciences [q-bio]DIVERSITYPROTEINFusarium verticillioidesmaizeSECONDARY METABOLISMgene clusterEpigenesis GeneticHistonesFUM8FusariumGene Expression Regulation FungalASPERGILLUSPromoter Regions Genetic2. Zero hungerGenetics0303 health sciencesHistone deacetylase inhibitorhistone acetylationAcetylationArticlesGeneral MedicineChromatinChromatinGENOMEHistoneMultigene Family[SDE]Environmental SciencesTrichostatin AEpigenetics; Fusarium verticillioides; fmonisin synthesismedicine.drugCONIDIATIONChromatin Immunoprecipitationmedicine.drug_classGenes FungalChIPBiologyGFPZea maysMicrobiologyFumonisinsChromatin remodeling03 medical and health sciencesmedicineEpigeneticsMolecular Biology030304 developmental biologyepigenetics030306 microbiologyCLUSTERFumonisins; epigenetics; Fusarium verticillioides; maize; histone acetylation; histone deacetylases; ChIP; Trichostatin A; FUM1; FUM21; FUM8; GFP; gene clusterMycotoxinsChromatin Assembly and DisassemblyFUM1Histone Deacetylase InhibitorsTrichostatin AAcetylationbiology.proteinChromatin immunoprecipitationhistone deacetylases
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Influences of histone deacetylase inhibitors and resveratrol on DNA repair and chromatin compaction

2013

Accessibility of DNA is a prerequisite for both DNA damage and repair. Therefore, the chromatin structure is expected to have major impact on both processes, with opposite consequences for the stability of the genome. To analyse the influence of chromatin compaction on the generation and repair of various types of DNA modifications, we modulated the global chromatin structure of AS52 Chinese hamster ovary cells and HeLa cells by treatment with either histone deacetylase inhibitors or resveratrol and measured the repair kinetics of (i) pyrimidine dimers induced by ultraviolet B, (ii) oxidised purines generated by photosensitisation and (iii) single-strand breaks induced by H2O2, using an alk…

DNA RepairUltraviolet RaysDNA damageDNA repairHealth Toxicology and MutagenesisCarbazolesCHO CellsHydroxamic AcidsToxicologyChromatin remodelingCricetulusStilbenesHistone H2AGeneticsmedicineAnimalsDeoxyribonuclease IHumansDNA Breaks Single-StrandedGenetics (clinical)EpigenomicsbiologyChemistryMolecular biologyChromatinCell biologyProliferating cell nuclear antigenChromatinHistone Deacetylase InhibitorsButyratesTrichostatin APyrimidine DimersResveratrolbiology.proteinHeLa Cellsmedicine.drugMutagenesis
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Lovastatin protects human endothelial cells from the genotoxic and cytotoxic effects of the anticancer drugs doxorubicin and etoposide

2006

Background and purpose: 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) are frequently used lipid-lowering drugs. Moreover, they exert pleiotropic effects on cellular stress responses and death. Here, we analysed whether lovastatin affects the sensitivity of primary human endothelial cells (HUVEC) to the anticancer drug doxorubicin. Experimental approach: We investigated whether pretreatment of HUVEC with low dose of lovastatin influences the cellular sensitivity to doxorubicin. To this end, cell viability, proliferation and apoptosis as well as DNA damage-triggered stress response were analysed. Key results: Lovastatin reduced the cytotoxic potency of doxorub…

DNA ReplicationCell SurvivalDNA damageApoptosisBiologyPharmacologypolycyclic compoundsmedicineHumansTopoisomerase II InhibitorsDoxorubicinLovastatinEtoposideEtoposideFluorescent DyesPharmacologyAntibiotics AntineoplasticReverse Transcriptase Polymerase Chain ReactionTopoisomeraseCell CycleEndothelial Cellsnutritional and metabolic diseasesAntimutagenic AgentsFibroblastsCell cycleResearch PapersAntineoplastic Agents PhytogenicDoxorubicinDrug Resistance NeoplasmHMG-CoA reductasebiology.proteinlipids (amino acids peptides and proteins)LovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsTopoisomerase-II InhibitorReactive Oxygen SpeciesFluorescein-5-isothiocyanateDNA Damagemedicine.drugBritish Journal of Pharmacology
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Ultraviolet light-induced apoptotic death is impaired by the HMG-CoA reductase inhibitor lovastatin.

2003

HMG-CoA reductase inhibitors (i.e., statins) attenuate C-terminal isoprenylation of Rho GTPases, thereby inhibiting UV-C-induced activation of c-Jun-N-terminal kinases/stress-activated protein kinases (JNKs/SAPKs). Inhibition of UV-C-triggered JNK/SAPK activation by lovastatin is due to inhibition of Rac-SEK1/MKK4-mediated phosphorylation of JNKs/SAPKs at Thr183/Tyr185. UV-C-stimulated phosphorylation of p38 kinase (Thr180/Tyr182) is also impaired by lovastatin. Cell killing provoked by UV-C irradiation was significantly inhibited by lovastatin. This was paralleled by a reduced frequency of chromosomal aberrations, accelerated recovery from UV-C-induced transient replication blockage, inhib…

DNA ReplicationUltraviolet Raysp38 mitogen-activated protein kinasesBiophysicsApoptosisCHO CellsBiochemistryp38 Mitogen-Activated Protein KinasesCricetinaemedicineUltraviolet lightAnimalsMitogen-Activated Protein Kinase 8LovastatinMolecular BiologyCaspasebiologyKinaseCell BiologyCell biologyrac GTP-Binding ProteinsEnzyme ActivationCell killingApoptosisCaspasesHMG-CoA reductasebiology.proteinLovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsMitogen-Activated Protein Kinasesmedicine.drugBiochemical and biophysical research communications
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Personalized management of dyslipidemias in patients with diabetes-it is time for a new approach (2022)

2022

AbstractDyslipidemia in patients with type 2 diabetes (DMT2) is one of the worst controlled worldwide, with only about 1/4 of patients being on the low-density lipoprotein cholesterol (LDL-C) target. There are many reasons of this, including physicians’ inertia, including diabetologists and cardiologists, therapy nonadherence, but also underusage and underdosing of lipid lowering drugs due to unsuitable cardiovascular (CV) risk stratification. In the last several years there is a big debate on the risk stratification of DMT2 patients, with the strong indications that all patients with diabetes should be at least at high cardiovascular disease (CVD) risk. Moreover, we have finally lipid lowe…

Diabetes Mellitus Type 2 / diagnosisDyslipidemias / drug therapyEndocrinology Diabetes and Metabolism610 Medicine & health2705 Cardiology and Cardiovascular MedicineCardiovascular risk Diabetes Individual therapy approach Lipid lowering therapy StatinsHumansIndividual therapy approachDyslipidemiasHypolipidemic AgentsDiabetes Mellitus Type 2 / epidemiologyDiabetesStatinsCholesterol LDLCardiovascular riskAtherosclerosisDyslipidemias / diagnosis2712 Endocrinology Diabetes and MetabolismDiabetes Mellitus Type 22724 Internal MedicineDyslipidemias / epidemiology10209 Clinic for CardiologyProprotein Convertase 9Diabetes Mellitus Type 2 / drug therapyCardiology and Cardiovascular MedicineLipid lowering therapy
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Synthesis of N-acyl Derivatives of Aminocombretastatin A-4 and Study of their Interaction with Tubulin and Downregulation of c-Myc.

2021

11 p.-9 fig.-4 tab.

Down-RegulationAntineoplastic AgentsMicrotubule dynamicsStructure-Activity RelationshipDownregulation and upregulationMicrotubuleTubulinCell Line TumorDrug DiscoveryHumansMTT assayAminocombretastatin A-4Cell ProliferationbiologyChemistryCell growthIn vitroTubulin ModulatorsMolecular Docking SimulationTubulinc-MycBiochemistryCell cultureDocking (molecular)biology.proteinDrug Screening Assays AntitumorAnti-proliferative activityAnti-mitoticMedicinal chemistry (Shariqah (United Arab Emirates))
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Lipid-lowering drug use in Italian primary care: effects of reimbursement criteria revision

2008

OBJECTIVE: To assess whether the prescribing pattern of lipid-lowering drugs (LLD) changed after reimbursement criteria revision in a general practice in southern Italy. METHODS: From the Caserta-1 Local Health Service database, 93 general practitioners (GPs) who had consistently sent data about their patients during the years 2003-2005 were recruited. Prevalence of use and incidence of new treatments were calculated for each year, stratified by three drug cohorts: statins, omega-3 fatty acids, and fibrates. Subanalyses by gender, age, and indication of use were performed. RESULTS: Overall, 1-year prevalence of LLD use increased from 2003 to 2004. After reimbursement criteria revision (Nove…

Drug Utilizationmedicine.medical_specialtyPediatricsStatinSettore MED/09 - Medicina Internamedicine.drug_classMEDLINEstatinsInternal medicineFatty Acids Omega-3EpidemiologyHumansMedicinePharmacology (medical)RosuvastatinLipid-lowering drug Statins Omega-3 fatty acids Prevalence of use General practiceClofibrateReimbursementUnsaturated fatty acidHypolipidemic AgentsPharmacologygeneral practiceprevalence of usePrimary Health Careomega-3 fatty acidsbusiness.industryIncidence (epidemiology)General Medicinelipid-lowering drugSettore MED/45 - Scienze Infermieristiche Generali Cliniche E PediatricheDrug UtilizationItalyInsurance Health ReimbursementSettore BIO/14 - FarmacologiaHydroxymethylglutaryl-CoA Reductase Inhibitorslipid-lowering drug; statins; omega-3 fatty acids; prevalence of use; general practicebusinessmedicine.drug
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