Search results for " Peptide Fragments"

showing 8 items of 8 documents

Angiotensin Receptor Neprilysin Inhibition Compared With Enalapril on the Risk of Clinical Progression in Surviving Patients With Heart Failure

2015

Background— Clinical trials in heart failure have focused on the improvement in symptoms or decreases in the risk of death and other cardiovascular events. Little is known about the effect of drugs on the risk of clinical deterioration in surviving patients. Methods and Results— We compared the angiotensin-neprilysin inhibitor LCZ696 (400 mg daily) with the angiotensin-converting enzyme inhibitor enalapril (20 mg daily) in 8399 patients with heart failure and reduced ejection fraction in a double-blind trial. The analyses focused on prespecified measures of nonfatal clinical deterioration. In comparison with the enalapril group, fewer LCZ696-treated patients required intensification of med…

Angiotensin receptorVascular damage Radboud Institute for Health Sciences [Radboudumc 16]receptorsTetrazolesheart failureAngiotensin-Converting Enzyme InhibitorsKaplan-Meier EstimateSacubitrilAngiotensin; Heart failure; Neprilysin; Receptors; Aminobutyrates; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Biomarkers; Double-Blind Method; Enalapril; Heart Failure; Humans; Kaplan-Meier Estimate; Natriuretic Peptide Brain; Neprilysin; Peptide Fragments; Risk Factors; Stroke Volume; Survivors; Tetrazoles; Treatment Outcome; Troponin; Disease Progression; Medicine (all); Cardiology and Cardiovascular Medicine; Physiology (medical)AngiotensinEnalaprilRisk FactorsEnalapril/therapeutic useNatriuretic Peptide BrainHeart Failure/bloodSurvivorsReceptorNeprilysinAminobutyrates: Systèmes cardiovasculaire & respiratoire [D03] [Sciences de la santé humaine]Troponin/bloodTroponinAngiotensin Receptor Antagonists/therapeutic useDrug CombinationsAngiotensin-Converting Enzyme Inhibitors/therapeutic useTreatment OutcomeTetrazoles/therapeutic useCardiologyDisease ProgressionValsartanNeprilysinHeart Failure/blood/drug therapy/physiopathologyCardiology and Cardiovascular Medicinemedicine.drugReceptormedicine.medical_specialtyHeart failureneprilysinAngiotensin Receptor Antagonistsreceptors angiotensinDouble-Blind MethodPhysiology (medical)Internal medicineRenin–angiotensin systemmedicineHumansheart failure neprilysin receptors angiotensinEnalaprilbusiness.industryBiphenyl CompoundsStroke Volumemedicine.diseasePeptide FragmentsEndocrinologyAminobutyrates/therapeutic useStroke Volume/physiologyHeart failureNatriuretic Peptide Brain/blood: Cardiovascular & respiratory systems [D03] [Human health sciences]businessNeprilysin/antagonists & inhibitorsPeptide Fragments/bloodSacubitril ValsartanBiomarkersBiomarkers/blood
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Hypoallergenic fragment of Par j 2 increases functional expression of Toll-like receptors in atopic children.

2006

Background: Parietaria judaica (Par j) is one of the main causes of allergy in the Mediterranean countries. The activation of Toll-like receptor 4 (TLR4) by lipopolysaccharide (LPS) inhibits nasal inflammation of atopic children. Objective:  To examine, in vivo and in vitro, the effect of recombinant Par j 2 (rPar j 2) and of its fragments (1–55 and 52–102) on atopic children. Methods:  We used skin prick test for in vivo evaluations. We assessed, in vitro, in peripheral blood mononuclear cells (PBMC), the effect of rPar j 2 and of the two fragments on neutrophil chemotaxis, on CD45RO, on TLR2 and TLR4 expression, on LPS binding and on interferon (IFN)-γ release, by a microchemotaxis chambe…

Hypersensitivity ImmediateMaleAdolescentImmunologyBiologyPeripheral blood mononuclear cellImmune systemPeptide FragmentIn vivoImmunology and AllergyHumansReceptorChildToll-Like ReceptorPlant ProteinsToll-like receptorAllergenToll-Like Receptors; Peptide Fragments; Humans; Allergens; Hypersensitivity Immediate; Child; Plant Proteins; Adolescent; Male; FemaleToll-Like ReceptorsPlant ProteinChemotaxisAllergensPeptide FragmentsTLR2ImmunologyTLR4FemaleHumanAllergy
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SV40 transformed fibroblasts recognize the same 140 kD fibronectin chemotactic fragment as non-transformed cells

1985

SV40-virus-transformed human embryonal fibroblasts show an enhanced chemotactic response to the glycoprotein fibronectin. However, they recognize the same chemotactic active region as non-transformed fibroblasts. The result suggests that an enhancement of chemotaxis by fibroblasts which have been transformed with Simian Virus 40 is due not to the utilization of further chemotactic domains in the molecule, but to an increased sensitivity of the cells to the chemoattractant.

virusesSimian virus 40BiologyVirus*Cell Transformation Viral Cells Cultured Chemotaxis/*drug effects Embryo Fibroblasts/physiology Fibronectins/*pharmacology Human Peptide Fragments/pharmacology Polyomavirus macacae/*physiologyCellular and Molecular NeurosciencemedicineHumansFibroblastMolecular BiologyCells CulturedPharmacologychemistry.chemical_classificationChemotaxisChemotaxisEmbryoCell BiologyFibroblastsCell Transformation ViralEmbryo MammalianVirologyPeptide FragmentsCell biologyFibronectinsSv40 virusFibronectinmedicine.anatomical_structurechemistryCell culturebiology.proteinMolecular MedicineGlycoprotein
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Thioflavin T templates amyloid β(1–40) conformation and aggregation pathway

2015

Aβ(1-40) peptide supramolecular assembly and fibril formation processes are widely recognized to have direct implications in the progression of Alzheimer's disease. The molecular basis of this biological process is still unknown and there is a strong need of developing effective strategies to control the occurring events. To this purpose the exploitation of small molecules interacting with Aβ aggregation represents one of the possible routes. Moreover, the use specific labeling has represented so far one of the most common and effective methods to investigate such a process. This possibility in turn rests on the reliability of the probe/labels involved. Here we present evidences of the effe…

Protein StructureSecondaryAβ(1–40) peptideAmyloidProtein ConformationMolecular Sequence DataBiophysicsSupramolecular chemistryMolecular Dynamics SimulationProtein aggregationProtein Aggregation PathologicalBiochemistryProtein Structure SecondarySupramolecular assemblyProtein Aggregateschemistry.chemical_compoundProtein structureAlzheimer DiseasePathologicalSecondary structureAβ(1-40) peptideHumansBenzothiazolesAmino Acid SequenceFluorescent DyesAmyloid beta-PeptidesProtein StabilityOrganic ChemistryAlzheimer's diseaseProtein AggregationSmall moleculePeptide FragmentsSettore FIS/07 - Fisica Applicata(Beni Culturali Ambientali Biol.e Medicin)Peptide ConformationAlzheimer's disease; Aβ(1–40) peptide; Protein aggregation; Protein conformation; Secondary structure; Thioflavin T; Alzheimer Disease; Amino Acid Sequence; Amyloid beta-Peptides; Fluorescence Recovery After Photobleaching; Fluorescent Dyes; Humans; Molecular Dynamics Simulation; Molecular Sequence Data; Peptide Fragments; Protein Aggregates; Protein Aggregation Pathological; Protein Conformation; Protein Multimerization; Protein Stability; Protein Structure Secondary; ThiazolesThiazolesBiophysicBiochemistrychemistryThioflavin TBiophysicsThioflavinProtein MultimerizationFluorescence Recovery After PhotobleachingBiophysical Chemistry
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Minimal Information About an Immuno-Peptidomics Experiment (MIAIPE)

2018

Minimal Information about an Immuno-Peptidomics Experiment (MIAIPE) is an initiative of the members of the Human Immuno-Peptidome Project (HIPP), an international program organized by the Human Proteome Organization (HUPO). The aim of the MIAIPE guidelines is to deliver technical guidelines representing the minimal information required to sufficiently support the evaluation and interpretation of immunopeptidomics experiments. The MIAIPE document has been designed to report essential information about sample preparation, mass spectrometric measurement and associated mass spectrometry (MS)-related bioinformatics aspects that are unique to immunopeptidomics and may not be covered by the genera…

Proteomics0301 basic medicineComputer scienceComputational biologyProteomicsBiochemistrySpecimen Handling03 medical and health sciencesStandardisation & GuidelinesHuman proteome projectHumansantigen processing and presentationDatabases ProteinMolecular Biology030102 biochemistry & molecular biologyHistocompatibility Antigens Class IHistocompatibility Antigens Class IIimmunopeptidomicsComputational BiologyMass spectrometricPeptide Fragmentsmajor histocompatibility complex3. Good health030104 developmental biologyComputational Biology/standards; Databases Protein; Histocompatibility Antigens Class I/analysis; Histocompatibility Antigens Class I/immunology; Histocompatibility Antigens Class I/metabolism; Histocompatibility Antigens Class II/analysis; Histocompatibility Antigens Class II/immunology; Histocompatibility Antigens Class II/metabolism; Humans; Peptide Fragments/analysis; Peptide Fragments/immunology; Peptide Fragments/metabolism; Proteomics/standards; Software; Specimen Handling/standards; antigen processing and presentation; immunopeptidomics; major histocompatibility complexSoftwareantigen processing and presentation; immunopeptidomics; major histocompatibility complex
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Efficacy and safety of bempedoic acid for the treatment of hypercholesterolemia: A systematic review and meta-analysis

2020

Background Bempedoic acid is a first-in-class lipid-lowering drug recommended by guidelines for the treatment of hypercholesterolemia. Our objective was to estimate its average effect on plasma lipids in humans and its safety profile. Methods and findings We carried out a systematic review and meta-analysis of phase II and III randomized controlled trials on bempedoic acid (PROSPERO: CRD42019129687). PubMed (Medline), Scopus, Google Scholar, and Web of Science databases were searched, with no language restriction, from inception to 5 August 2019. We included 10 RCTs (n = 3,788) comprising 26 arms (active arm [n = 2,460]; control arm [n = 1,328]). Effect sizes for changes in lipids and high-…

Apolipoprotein BPublication Ethics030204 cardiovascular system & hematologyCardiovascularGastroenterologyLipoprotein particleMedical and Health SciencesBiochemistrychemistry.chemical_compoundDatabase and Informatics Methods0302 clinical medicineMathematical and Statistical TechniquesAnticholesteremic Agents Apolipoproteins B Cholesterol Cholesterol LDL Clinical Trials Phase II as Topic Clinical Trials Phase III as Topic Dicarboxylic Acids Fatty Acids Humans Hypercholesterolemia Peptide Fragments Randomized Controlled Trials as TopicLipid and Blood Pressure Meta-Analysis Collaboration (LBPMC) Group and the International Lipid Expert PanelMedicine and Health SciencesDicarboxylic Acids030212 general & internal medicineDatabase SearchingResearch IntegrityRandomized Controlled Trials as Topicmedicine.diagnostic_testbiologyAnticholesteremic AgentsStatisticsFatty AcidsRDrugsGeneral MedicineMetaanalysisSerious Mental IllnessLipidsPhase III as TopicMental HealthCholesterolPhysical SciencesMedicineResearch Articlemedicine.medical_specialtyRMScience PolicyLipoproteinsHypercholesterolemiaBempedoic acid hypercholesterolemia lipid profile hsCRPResearch and Analysis MethodsLDL03 medical and health sciencesClinical Trials Phase II as TopicInternal medicineGeneral & Internal MedicinemedicineHumansClinical TrialsStatistical MethodsApolipoproteins BPharmacologyPlasma Proteinsbusiness.industryCholesterolPhase II as TopicStatinsBiology and Life SciencesProteinsOdds ratioCholesterol LDLConfidence intervalPeptide FragmentschemistryClinical Trials Phase III as Topicbiology.proteinUric acidCreatine kinaseLipid profilebusinessDigestive DiseasesMathematicsPLoS Medicine
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Oxidative signature of cerebrospinal fluid from mild cognitive impairment and Alzheimer disease patients

2015

Abstract Background Several studies suggest that pathological changes in Alzheimer’s disease (AD) brain begin around 10–20 years before the onset of cognitive impairment. Biomarkers that can support early diagnosis and predict development of dementia would, therefore, be crucial for patient care and evaluation of drug efficacy. Although cerebrospinal fluid (CSF) levels of Aβ42, tau, and p-tau are well-established diagnostic biomarkers of AD, there is an urgent need to identify additional molecular alterations of neuronal function that can be evaluated at the systemic level. Objectives This study was focused on the analysis of oxidative stress-related modifications of the CSF proteome, from …

0301 basic medicineOncologyPathologyDiseasephysiology (medical)medicine.disease_causeProtein oxidationtau proteins0302 clinical medicineCerebrospinal fluidmiddle aged80 and overoxidative stresshumansAged 80 and overamyloid beta-peptidesredox proteomicsagedfemale030220 oncology & carcinogenesisBiomarker (medicine)Alzheimer's diseaseAlzheimer diseaseAPOEmedicine.medical_specialtyoxidation-reductionproteomeCSFmolecular sequence data03 medical and health sciencesmalecognitive dysfunctionInternal medicinemental disordersmedicineDementiabiochemistryprotein oxidationbusiness.industrypeptide fragmentscase-control studiesCase-control studybiomarkersmedicine.diseaseAPOE; biomarkers; CSF; extracellular chaperones; protein oxidation; redox proteomics; aged; aged 80 and over; Alzheimer disease; amino acid sequence; amyloid beta-peptides; apolipoproteins E; biomarkers; case-control studies; cognitive dysfunction; female; humans; male; middle aged; molecular sequence data; oxidation-reduction; oxidative stress; peptide fragments; proteome; tau proteins; biochemistry; physiology (medical)extracellular chaperonesamino acid sequence030104 developmental biologybusinessOxidative stressapolipoproteins E
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Exacerbated experimental autoimmune encephalomyelitis in mast-cell-deficient KitW-sh/W-sh mice

2011

Mast cell (MC)-deficient c-Kit mutant Kit(W/W-v) mice are protected against experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, suggesting a detrimental role for MCs in this disease. To further investigate the role of MCs in EAE, we took advantage of a recently characterized model of MC deficiency, Kit(W-sh/W-sh). Surprisingly, we observed that myelin oligodendrocyte glycoprotein (MOG)(35-55)-induced chronic EAE was exacerbated in Kit(W-sh/W-sh) compared with Kit(+/+) mice. Kit(W-sh/W-sh) mice showed more inflammatory foci in the central nervous system (CNS) and increased T-cell response against myelin. To understand whether the discrepant results obtaine…

Central Nervous SystemT-LymphocytesEncephalomyelitisexperimental autoimmune encephalomyelitismast cellsInbred C57BLSeverity of Illness IndeximmunologyMiceMyelinPeptide Fragmentimmune system diseasesMast CellEncephalomyelitisMyelin SheathbiologyExperimental autoimmune encephalomyelitisMast cellProto-Oncogene Proteins c-kitPhenotypemedicine.anatomical_structuremastcell-deficient miceBone Marrow Cellgenetics/immunology/pathology/prevention /&/ controlc-kit mutationsc-kit mutations; experimental autoimmune encephalomyelitis; granulocytes; mast cellsEncephalomyelitis Autoimmune ExperimentalCentral nervous systemBone Marrow CellsPathology and Forensic MedicineMyelin oligodendrocyte glycoproteinExperimentalAnimals Antibody Formation Bone Marrow Cells; pathology Central Nervous System; pathology Encephalomyelitis; Autoimmune; Experimental; genetics/immunology/pathology/prevention /&/ control Glycoproteins; immunology Granulocytes; pathology Immunization Mast Cells; pathology Mice Mice; Inbred C57BL Mutation Myelin Sheath; immunology Myelin-Oligodendrocyte Glycoprotein Peptide Fragments; immunology Phenotype Proto-Oncogene Proteins c-kit; deficiency/genetics/metabolism Severity of Illness Index T-Lymphocytes; pathologyAntigendeficiency/genetics/metabolismmedicineAnimalsMolecular BiologyGlycoproteinsAnimalMultiple sclerosismast-cell-deficient Kit W-sh/W-sh mice.Experimental autoimmune encephalomyelitis; mast-cell-deficient Kit W-sh/W-sh mice.GranulocytegranulocytesCell Biologymedicine.diseaseEncephalomyelitiExperimental autoimmune encephalomyelitiPeptide FragmentsMice Inbred C57BLT-LymphocyteAntibody FormationMutationImmunologybiology.proteinexperimental autoimmune encephalomyelitis; mastcell-deficient mice; mast cellspathologyImmunizationMyelin-Oligodendrocyte GlycoproteinGlycoproteinAutoimmuneLaboratory Investigation
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