Search results for "Niacin"

showing 10 items of 89 documents

Impact of Individual Components of the Metabolic Syndrome on the Outcome of Patients with Advanced Hepatocellular Carcinoma Treated with Sorafenib

2017

<b><i>Background/Aim:</i></b> Individual components of the metabolic syndrome (MS) such as obesity or diabetes mellitus impair the prognosis of patients with hepatocellular carcinoma (HCC) following curative treatment approaches or transarterial therapies. The aim of this retrospective study was to assess the impact of these factors on the overall survival (OS) of patients with advanced HCC treated with sorafenib. <b><i>Methods:</i></b> Univariate and multivariate analyses were performed to assess the impact of individual components of the MS on the OS of 152 consecutive patients with advanced HCC treated with sorafenib. <b><i>Resu…

AdultMaleNiacinamideOncologySorafenibmedicine.medical_specialtyCarcinoma HepatocellularAntineoplastic AgentsYoung Adult03 medical and health sciences0302 clinical medicineDiabetes mellitusInternal medicinemedicineHumansSurvival analysisAgedNeoplasm StagingProportional Hazards ModelsRetrospective StudiesAged 80 and overMetabolic Syndromebusiness.industryProportional hazards modelPhenylurea CompoundsLiver NeoplasmsHazard ratioGastroenterologyGeneral MedicineMiddle AgedSorafenibPrognosismedicine.diseaseSurvival Analysisdigestive system diseasesTreatment OutcomeDiabetes Mellitus Type 2030220 oncology & carcinogenesisHepatocellular carcinomaMultivariate AnalysisFemale030211 gastroenterology & hepatologyMetabolic syndromebusinessDyslipidemiamedicine.drugDigestive Diseases
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Nitric oxide production and endothelium-dependent vasorelaxation ameliorated by N1-methylnicotinamide in human blood vessels.

2012

N 1 -methylnicotinamide (MNA + ) has until recently been thought to be a biologically inactive product of nicotinamide metabolism in the pyridine nucleotides pathway. However, the latest observations imply that MNA + may exert antithrombotic and anti-inflammatory effects through direct action on the endothelium. We examined both in vivo and in vitro whether the compound might induce vasorelaxation in human blood vessels through the improvement of nitric oxide (NO) bioavailability and a reduction of oxidative stress mediated by endothelial NO synthase (eNOS) function. MNA + treatment (100 mg/m 2 orally) in healthy normocholesterolemic and hypercholesterolemic subjects increased the l-argini…

AdultNiacinamidemedicine.medical_specialtyEndotheliumBrachial ArteryNitric Oxide Synthase Type IIIHypercholesterolemiachemistry.chemical_elementCalciumIn Vitro Techniquesmedicine.disease_causeNitric OxideNitric oxidechemistry.chemical_compoundN^{1}-methylnicotinamideDouble-Blind MethodEnosnitric oxideInternal medicineInternal MedicinemedicineHumansflow-mediated dilationCalcimycinCells Culturedendothelial nitric oxide synthaseoxidized low-density lipoproteinbiologyDose-Response Relationship DrugChemistrySuperoxidebiology.organism_classificationendothelial cellsAcetylcholineOxygenVasodilationOxidative Stressmedicine.anatomical_structureEndocrinologysuperoxideEndothelium VascularAcetylcholineOxidative stressmedicine.drugLipoproteinHypertension (Dallas, Tex. : 1979)
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Effects of oral niacin on endothelial dysfunction in patients with coronary artery disease: Results of the randomized, double-blind, placebo-controll…

2009

High-density-lipoproteins-cholesterol (HDL-C) is invertedly related to the incidence of cardiovascular events. Recent studies suggest that HDL-C directly improves endothelial function. Nicotinic acid (niacin) effectively raises serum HDL-C. We therefore hypothesized that treatment with niacin improves endothelial dysfunction in patients with coronary artery disease (CAD). One hundred seven patients with CAD were randomly assigned to double-blinded treatment for 12 weeks with extended-release (ER)-niacin 1000 mg/day (N) or placebo (C), respectively. Flow-mediated dilation (FMD) of the brachial artery, nitroglycerin-mediated endothelium-independent dilation (NMD) and serum lipid concentration…

Blood GlucoseMalemedicine.medical_specialtyBrachial ArteryVasodilator AgentsAdministration OralCoronary Artery DiseasePlaceboNiacinGastroenterologyCoronary artery diseaseNitroglycerinchemistry.chemical_compoundHigh-density lipoproteinDouble-Blind MethodInternal medicinemedicine.arterymedicineHumansProspective StudiesPhosphorylationEndothelial dysfunctionBrachial arteryTriglyceridesAgedUltrasonographyVascular diseasebusiness.industryCholesterol HDLMicrofilament Proteinsnutritional and metabolic diseasesCholesterol LDLMiddle AgedPhosphoproteinsmedicine.diseaseVasodilationB vitaminsTreatment OutcomeEndocrinologychemistryDelayed-Action PreparationsFemalelipids (amino acids peptides and proteins)Endothelium VascularCardiology and Cardiovascular MedicinebusinessCell Adhesion MoleculesBiomarkersNiacinAtherosclerosis
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Refining sorafenib therapy: lessons from clinical practice

2015

ABSTRACT  Understanding the best use of sorafenib is essential in order to maximize clinical benefit in hepatocellular carcinoma. Based on Phase III and noninterventional study data, as well as our extensive experience, we discuss dose modification in order to manage adverse events, disease response evaluation and how to maximize treatment benefit. Sorafenib should be initiated at the approved dose (400 mg twice daily) and reduced/interrupted as appropriate in order to manage adverse events. Dose modification should be considered before discontinuation. Appropriate tumor response assessment is critical. Focusing on radiologic response may result in premature sorafenib discontinuation; symp…

Cancer ResearchSettore SECS-P/06 - Economia ApplicataAntineoplastic AgentAge FactorChild–Pugh Bpostprogression treatmentresponse assessmentdose modificationClinical Trials as TopicLiver Neoplasmsadverse event managementAge FactorsChild-Pugh Bpostprogression treatmenthepatocellular carcinomaGeneral MedicinePrognosisadverse event management; child–Pugh B; dose modification; elderly hepatocellular carcinoma; mRECIST; postprogression treatment; eal-world data; response assessment; sorafenibelderly hepatocellular carcinomaCombined Modality Therapychild–Pugh BClinical PracticeTreatment OutcomeOncologyLiver Neoplasmeal-world dataHepatocellular carcinomaadverse event managementRetreatmentDisease Progressiondose modificationHumanmedicine.drugPhenylurea CompoundNiacinamideSorafenibmedicine.medical_specialtyCarcinoma HepatocellularDisease ResponsePrognosielderly hepatocellular carcinomaProtein Kinase InhibitorAntineoplastic AgentsmRECISTelderlymRECISTAdverse event management Child–Pugh B dose modification elderly hepatocellular carcinoma mRECIST postprogression treatment real-world data response assessment sorafenibmedicineChild–Pugh BHumansCombined Modality TherapyIntensive care medicineAdverse effectProtein Kinase InhibitorsDose Modificationreal-world databusiness.industryPhenylurea Compoundsmedicine.diseaseDiscontinuationSurgeryreal-world dataresponse assessmentsorafenibbusinessFuture Oncology
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Preclinical and clinical evidence of activity of pazopanib in solitary fibrous tumour

2014

Abstract Background To explore the activity of pazopanib in solitary fibrous tumour (SFT). Patients and methods In a preclinical study, we compared the activity of pazopanib, sorafenib, sunitinib, regorafenib, axitinib and bevacizumab in a dedifferentiated-SFT (DSFT) xenotransplanted into Severe Combined Immunodeficiency (SCID) mice. Antiangiogenics were administered at their reported optimal doses when mean tumour volume (TV) was 80 mm3. Drug activity was assessed as TV inhibition percentage (TVI%). From May 2012, six consecutive patients with advanced SFT received pazopanib, on a national name-based programme. In one case sunitinib was administered after pazopanib failure. Results In the …

Chemotherapy; Pazopanib; Sarcoma; Solitary fibrous tumour; Sunitinib; Tyrosine kinase; Administration Oral; Adult; Aged; Angiogenesis Inhibitors; Animals; Antibodies Monoclonal Humanized; Antineoplastic Agents; Bevacizumab; Humans; Imidazoles; Indazoles; Indoles; MAP Kinase Signaling System; Male; Mice SCID; Middle Aged; Neoplasm Transplantation; Niacinamide; Phenylurea Compounds; Pyridines; Pyrimidines; Pyrroles; Receptor Platelet-Derived Growth Factor beta; Solitary Fibrous Tumors; Sulfonamides; Transplantation Heterologous; Vascular Endothelial Growth Factor Receptor-2; Cancer Research; Oncology; Medicine (all)OncologyMaleCancer ResearchIndolesAxitinibPyridinesPyridinemedicine.medical_treatmentSolitary fibrous tumourAdministration OralAngiogenesis InhibitorsMice SCIDPharmacologyPyrroleAntineoplastic Agentchemistry.chemical_compoundMiceSolitary Fibrous TumorChemotherapy; Pazopanib; Sarcoma; Solitary fibrous tumour; Sunitinib; Tyrosine kinase; Cancer Research; Oncology; Medicine (all)Transplantation HeterologouMonoclonalSunitinibHumanizedSulfonamidesHeterologousSunitinibMedicine (all)ImidazolesSarcomaMiddle AgedSorafenibPlatelet-Derived Growth Factor betaAxitinibBevacizumabOncologySolitary Fibrous TumorsAdministrationAngiogenesis InhibitorHumanmedicine.drugReceptorPhenylurea CompoundSorafenibOralAdultNiacinamidemedicine.medical_specialtyIndazolesBevacizumabMAP Kinase Signaling SystemTransplantation HeterologousAntineoplastic AgentsSulfonamideAntibodies Monoclonal HumanizedSCIDAntibodiesReceptor Platelet-Derived Growth Factor betaPazopanibInternal medicineRegorafenibmedicineAnimalsHumansChemotherapyPyrrolesImidazoleTyrosine kinaseAgedChemotherapyTransplantationAnimalbusiness.industryPhenylurea CompoundsPazopanibmedicine.diseaseChemotherapy; Pazopanib; Sarcoma; Solitary fibrous tumour; Sunitinib; Tyrosine kinase; Administration Oral; Adult; Aged; Angiogenesis Inhibitors; Animals; Antibodies Monoclonal Humanized; Antineoplastic Agents; Axitinib; Bevacizumab; Humans; Imidazoles; Indazoles; Indoles; MAP Kinase Signaling System; Male; Mice SCID; Middle Aged; Neoplasm Transplantation; Niacinamide; Phenylurea Compounds; Pyridines; Pyrimidines; Pyrroles; Receptor Platelet-Derived Growth Factor beta; Solitary Fibrous Tumors; Sorafenib; Sulfonamides; Sunitinib; Transplantation Heterologous; Vascular Endothelial Growth Factor Receptor-2Vascular Endothelial Growth Factor Receptor-2IndazolePyrimidinesPyrimidinechemistryIndolebusinessProgressive diseaseNeoplasm Transplantation
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Multiple modes of cell death in neuroendocrine tumors induced by artesunate.

2020

Abstract Background The paucity of effective treatment in neuroendocrine tumors (NETs) encouraged us to investigate the therapeutic value of artesunate (ART) promised by its inhibitory effect against various tumors and broad safety profile. Methods We evaluated the impact of ART on three NET cell lines, BON-1, QGP-1 and NCI-H727 on cellular and molecular levels. Results Our results showed that ART induced endoplasmic reticulum (ER) stress through phosphorylation of eIF2α, which further gave rise to autophagy in all three NET cell lines. Specifically, apoptosis and ferroptosis were also observed in BON-1 cells, which made BON-1 cell line more vulnerable upon ART treatment. The different sens…

Cyclin-Dependent Kinase Inhibitor p21NiacinamideProgrammed cell deathPharmaceutical ScienceArtesunateAntineoplastic AgentsApoptosisNeuroendocrine tumorsBiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDownregulation and upregulationCell Line TumorDrug DiscoveryAntineoplastic Combined Chemotherapy ProtocolsmedicineAutophagyFerroptosisHumans030304 developmental biologyPharmacology0303 health sciencesEndoplasmic reticulumPhenylurea CompoundsAutophagymedicine.diseaseEndoplasmic Reticulum StressNeuroendocrine TumorsComplementary and alternative medicinechemistryCell cultureApoptosisArtesunate030220 oncology & carcinogenesisCancer researchMolecular MedicinePhytomedicine : international journal of phytotherapy and phytopharmacology
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Metal ions modify DNA-protecting and mutagen-scavenging capacities of the AV-153 1,4-dihydropyridine.

2019

Abstract 1,4-Dihydropyridines (1,4-DHP) possess important biochemical and pharmacological properties, including antioxidant and antimutagenic activities. AV-153-Na, an antimutagenic and DNA-repair enhancing compound was shown to interact with DNA by intercalation. Here we studied DNA binding of several AV-153 salts to evaluate the impact of AV-153 modifications on its DNA binding capacity, the ability to scavenge the peroxynitrite, to protect HeLa and B-cells cells against DNA damage. Affinity of the AV-153 salts to DNA measured by a fluorescence assay was dependent on the metal ion forming a salt in position 4 of the 1,4-DHP, and it decreased as follows: Mg > Na > Ca > Li > Rb > K. AV-153-…

DihydropyridinesAntioxidantDNA RepairDNA damageHealth Toxicology and Mutagenesismedicine.medical_treatmentMetal ions in aqueous solutionIntercalation (chemistry)[SDV.CAN]Life Sciences [q-bio]/CancerMutagen02 engineering and technologymedicine.disease_causeNiacinAntioxidantsHeLa03 medical and health scienceschemistry.chemical_compoundPeroxynitrous AcidGeneticsmedicineHumansDrug InteractionsDNA Breaks Single-StrandedComputingMilieux_MISCELLANEOUS030304 developmental biology0303 health sciencesB-Lymphocytesbiology021001 nanoscience & nanotechnologybiology.organism_classificationIntercalating AgentsRecombinant ProteinsOxidative StresschemistryMetalsBiophysicstat Gene Products Human Immunodeficiency VirusComet AssaySingle-Cell Analysis0210 nano-technologyDNAPeroxynitriteDNA DamageHeLa CellsMutation research. Genetic toxicology and environmental mutagenesis
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DNA-binding studies of AV-153, an antimutagenic and DNA repair-stimulating derivative of 1,4-dihydropiridine.

2014

Abstract The ability to intercalate between DNA strands determines the cytotoxic activity of numerous anticancer drugs. Strikingly, intercalating activity was also reported for some compounds considered to be antimutagenic. The aim of this study was to determine the mode of interaction of DNA with the antimutagenic and DNA repair-stimulating dihydropyridine (DHP) AV-153. DNA and AV-153 interactions were studied by means of UV/VIS spectroscopy, fluorimetry and infrared spectroscopy. Compound AV-153 is a 1,4 dihydropyridine with ethoxycarbonyl groups in positions 3 and 5. Computer modeling of AV-153 and DNA interactions suggested an ability of the compound to dock between DNA strands at a sin…

DihydropyridinesBinding SitesDNA RepairMolecular StructureGuanineDNA repairStereochemistryAntimutagenic AgentsGeneral MedicineDNAToxicologyNiacinThymineRatschemistry.chemical_compoundPlasmidDNA IntercalationchemistryLiverSpectroscopy Fourier Transform InfraredAnimalsA-DNACytosineDNAChemico-biological interactions
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LDL and HDL subfractions, dysfunctional HDL: treatment options.

2014

Low-density lipoproteins (LDL) are considered as important risk factors for cardiovascular diseases (CVD), while highdensity lipoproteins (HDL) are well recognized for their putative role in reverse cholesterol transport and other atheroprotective functions. Both LDL and HDL are heterogeneous in nature, including various subfractions depending on the method of isolation (≥ 7 LDL and 10 HDL subspecies, respectively). While it is established that small, dense LDL (sdLDL) have atherogenic potential, the role of different HDL subfractions is still largely unclear. The majority of clinical studies suggest an atheroprotective role of larger HDL particles, although recent work has highlighted the…

Drugmedicine.medical_specialtymedia_common.quotation_subjectDysfunctional familychemistry.chemical_compoundRisk FactorsInternal medicineDrug DiscoveryCholesterylester transfer proteinmedicineHumansmedia_commonPharmacologybiologybusiness.industryCholesterolReverse cholesterol transportnutritional and metabolic diseasesLipoproteins LDLResidual riskEndocrinologychemistryCardiovascular Diseasesbiology.proteinlipids (amino acids peptides and proteins)Hdl subfractionsHydroxymethylglutaryl-CoA Reductase InhibitorsLipoproteins HDLbusinessNiacin
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Fatty Liver and Fibrosis in Glycine N-Methyltransferase Knockout Mice Is Prevented by Nicotinamide

2010

Deletion of glycine N-methyltransferase (GNMT), the main gene involved in liver S-adenosylmethionine (SAM) catabolism, leads to the hepatic accumulation of this molecule and the development of fatty liver and fibrosis in mice. To demonstrate that the excess of hepatic SAM is the main agent contributing to liver disease in GNMT knockout (KO) mice, we treated 1.5-month-old GNMT-KO mice for 6 weeks with nicotinamide (NAM), a substrate of the enzyme NAM N-methyltransferase. NAM administration markedly reduced hepatic SAM content, prevented DNA hypermethylation, and normalized the expression of critical genes involved in fatty acid metabolism, oxidative stress, inflammation, cell proliferation, …

Liver CirrhosisNiacinamidemedicine.medical_specialtyPathologyS-AdenosylmethionineCirrhosisGene ExpressionGlycine N-MethyltransferaseBiologyArticleLiver diseasechemistry.chemical_compoundMiceFibrosisInternal medicinemedicineAnimalsRas signalingMice KnockoutDNA methylationHepatologyFatty acid metabolismFatty livermedicine.diseaseGlycine N-methyltransferaseFatty LiverEndocrinologyJAK/STAT signalingchemistryGNMThepatocytesHepatic fibrosisGene Deletion
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