Search results for "DISEASE PROGRESSION"

showing 10 items of 835 documents

The use of Stokes-Mueller polarimetry for assessment of amyloid-β progression in a mouse model of Alzheimer’s disease

2020

Abstract Alzheimer’s disease, being a major societal burden, demands improvement of current techniques for its treatment and diagnostics. Currently only autopsy histology is able to provide the definite diagnosis for Alzheimer’s disease. However, the procedure is rather time consuming and costly. In the current study, we utilized Stokes and Mueller polarimetry techniques to screen for amyloid-β (Aβ) deposits in formalin-fixed, paraffin-embedded mouse brain tissue at different stages of Alzheimer’s disease. The study has shown that the presence of Aβ plaques influences the properties of scattered polarized light. The Poincaré sphere was used as a graphical tool for the visualization of the a…

Amyloid βbrainPolarimetryDiseaselight scatteringScattering03 medical and health sciencessymbols.namesake0302 clinical medicinestatistical analysisScreening methodStokes parameterstissuesComputingMilieux_MISCELLANEOUS030304 developmental biologyPoincare spherepolarimetryPhysics0303 health sciencespolarizationDisease progressionDepolarizationAlzheimer's diseaseAlzheimer's[SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsStatistical analysisAmyloid-ß plaque[SPI.OPTI]Engineering Sciences [physics]/Optics / PhotonicsymbolsAnisotropyDepolarizationNeuroscience030217 neurology & neurosurgeryOptical Biopsy XVIII: Toward Real-Time Spectroscopic Imaging and Diagnosis
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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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Macrophage Migration Inhibitory Factor Induces Inflammation and Predicts Spinal Progression in Ankylosing Spondylitis

2017

Objective: To investigate the role of macrophage migration inhibitory factor (MIF) in the pathogenesis of ankylosing spondylitis (AS). Methods: Patients who met the modified New York criteria for AS were recruited for the study. Healthy volunteers, rheumatoid arthritis patients, and osteoarthritis patients were included as controls. Based on the annual rate of increase in modified Stoke AS Spine Score (mSASSS), AS patients were classified as progressors or nonprogressors. MIF levels in serum and synovial fluid were quantitated by enzyme-linked immunosorbent assay. Predictors of AS progression were evaluated using logistic regression analysis. Immunohistochemical analysis of ileal tissue was…

AnkylosingAdultMaleLogistic ModelMacrophageImmunologyEnzyme-Linked Immunosorbent AssayIntramolecular OxidoreductasePredictive Value of TestMonocyteSeverity of Illness IndexCalcificationCalcification PhysiologicPaneth CellRheumatologySynovial Fluidotorhinolaryngologic diseasesImmunology and AllergySpondylitis AnkylosingPhysiologicSpondylitiMacrophage Migration-Inhibitory FactorTumor Necrosis Factor-alphaOsteoblastB-LymphocyteHistocompatibility Antigens Class IIMiddle AgedSpineAntigens Differentiation B-LymphocyteSettore MED/16 - ReumatologiaAntigenDifferentiationDisease ProgressionFemaleCase-Control StudieHuman
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Deficiency of glutathione peroxidase-1 accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice.

2007

Background— We have recently demonstrated that activity of red blood cell glutathione peroxidase-1 is inversely associated with the risk of cardiovascular events in patients with coronary artery disease. The present study analyzed the effect of glutathione peroxidase-1 deficiency on atherogenesis in the apolipoprotein E-deficient mouse. Methods and Results— Female apolipoprotein E-deficient mice with and without glutathione peroxidase-1 deficiency were placed on a Western-type diet for another 6, 12, or 24 weeks. After 24 weeks on Western-type diet, double-knockout mice (GPx-1 −/− ApoE −/− ) developed significantly more atherosclerosis than control apolipoprotein E-deficient mice. Moreover…

Apolipoprotein Emedicine.medical_specialtyGPX1AntioxidantApolipoprotein Bmedicine.medical_treatmentLipoproteinsApoptosisBlood Pressuremedicine.disease_causeNitric OxideMitochondria HeartMonocyteschemistry.chemical_compoundMiceApolipoproteins EGlutathione Peroxidase GPX1SuperoxidesInternal medicinePeroxynitrous AcidmedicineAnimalsAortaCell Proliferationchemistry.chemical_classificationMice KnockoutReactive oxygen speciesGlutathione PeroxidaseMembranesbiologyGlutathione peroxidaseGlutathioneAtherosclerosisEndocrinologyPhenotypechemistryImmunologybiology.proteinDisease ProgressionFemaleCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidation-ReductionOxidative stressArteriosclerosis, thrombosis, and vascular biology
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Immunopathogenesis of atherosclerosis: endotoxin accelerates atherosclerosis in rabbits on hypercholesterolemic diet.

2001

Background—On the basis of our concept that atherosclerosis has an immunopathological background, we tested whether activation of the innate immune system influences its progression.Methods and Results—Hypercholesterolemic (0.5% wt/wt diet) rabbits received either repeated intravenous injections of endotoxin (Escherichia colilipopolysaccharide 1.25 to 2.5 μg, once per week) or a self-limiting cutaneousStaphylococcus aureusinfection with or without a quinolone antibiotic. Measured laboratory parameters, including LDL and HDL cholesterols, were similar in the different groups of hypercholesterolemic animals. All endotoxin-treated animals developed transient episodes of fever after endotoxin a…

ArteriosclerosisInnate immunologyHypercholesterolemiaTriglycerides bloodPathogenesisCholesterol Dietarychemistry.chemical_compoundImmunityPhysiology (medical)MedicineAnimalsAortaTriglyceridesInnate immune systemCholesterolbusiness.industryDisease progressionCholesterol HDLCholesterol LDLImmunity InnateCholesterol bloodEndotoxinsDisease Models AnimalCholesterolchemistryImmunologyDisease ProgressionDiet AtherogenicFemaleStaphylococcal Skin InfectionsRabbitsCardiology and Cardiovascular MedicinebusinessCirculation
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The matricellular protein SPARC supports follicular dendritic cell networking toward Th17 responses.

2011

Abstract Lymphnode swelling during immune responses is a transient, finely regulated tissue rearrangement, accomplished with the participation of the extracellular matrix. Here we show that murine and human reactive lymph nodes express SPARC in the germinal centres. Defective follicular dendritic cell networking in SPARC-deficient mice is accompanied by a severe delay in the arrangement of germinal centres and development of humoral autoimmunity, events that are linked to Th17 development. SPARC is required for the optimal and rapid differentiation of Th17 cells, accordingly we show delayed development of experimental autoimmune encephalomyelitis whose pathogenesis involves Th17. Not only h…

Autoimmune diseases; Extracellular matrix; Germinal centre reaction; Th17 cellsEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisImmunologyCell CommunicationBiologyfollicular dendritic cellExtracellular matrixAnimals Genetically ModifiedMiceImmune systemSPARC; follicular dendritic cell; Th17Autoimmune diseasemedicinegerminal centre reactionImmunology and AllergyAnimalsHumansautoimmune diseasesOsteonectinMice KnockoutB-LymphocytesCD40Follicular dendritic cellsExperimental autoimmune encephalomyelitisMatricellular proteinGerminal centerSPARCCell Differentiationmedicine.diseaseCell biologyExtracellular MatrixImmunity HumoralMice Inbred C57BLCrosstalk (biology)Disease Models AnimalImmunologybiology.proteinDisease ProgressionTh17 CellsImmunizationMyelin-Oligodendrocyte GlycoproteinTh17autoimmune diseases; extracellular matrix; germinal centre reaction; th17 cellsDendritic Cells FollicularMyelin ProteinsJournal of autoimmunity
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GSK-3? Can Regulate the Sensitivity of MIA-PaCa-2 Pancreatic and MCF-7 Breast Cancer Cells to Chemotherapeutic Drugs, Targeted Therapeutics and Nutra…

2021

Glycogen synthase kinase-3 (GSK-3) is a regulator of signaling pathways. KRas is frequently mutated in pancreatic cancers. The growth of certain pancreatic cancers is KRas-dependent and can be suppressed by GSK-3 inhibitors, documenting a link between KRas and GSK-3. To further elucidate the roles of GSK-3β in drug-resistance, we transfected KRas-dependent MIA-PaCa-2 pancreatic cells with wild-type (WT) and kinase-dead (KD) forms of GSK-3β. Transfection of MIA-PaCa-2 cells with WT-GSK-3β increased their resistance to various chemotherapeutic drugs and certain small molecule inhibitors. Transfection of cells with KD-GSK-3β often increased therapeutic sensitivity. An exception was observed wi…

Berberineendocrine system diseasesmedicine.medical_treatmentRegulatormedicine.disease_causeDeoxycytidinePiperazinesTargeted therapychemotherapeutic drugsTargeted therapyNitrophenolsBreast cancerGSK-3BGlycolysisMolecular Targeted TherapyNeoplasm Metastasistargeted therapy;lcsh:QH301-705.5Tumor Stem Cell AssaySulfonamidesTumorbiologyChemistryGeneral MedicineTransfectionMetforminDisease ProgressionMCF-7 CellsFemaleKRASNutraceuticalsFluorouracilSignal transductionGlycolysisSignal TransductionBCL2bcl-X ProteinAntineoplastic AgentsBreast Neoplasmsmacromolecular substancesAdenocarcinomaArticleCell LineInhibitory Concentration 50Cell Line TumorThiadiazolesmedicineDiabetes MellitusKRasHumansGlycogen synthaseProtein Kinase InhibitorsCell ProliferationChemotherapeu-tic drugsGlycogen Synthase Kinase 3 betaGSK-3βAdenylate KinaseBiphenyl Compoundsnutraceuticals;PDACβ-cateninGemcitabine?-cateninMalariaPancreatic Neoplasmslcsh:Biology (General)MCF-7DoxorubicinDietary SupplementsCancer researchbiology.protein
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The potential use of biomarkers as an adjunctive tool for staging bipolar disorder

2009

Recent data show that biomarkers differ in early and late-stage bipolar disorder (BD). Here we propose a model of staging for bipolar disorder that emphasizes the potential use of biomarkers for differentiating early and late-stage BD patients in the inter-episodic period. The proposed model includes a Latent phase: patients at "ultra-high-risk" for developing BD, characterized by a family history of BD, temperament traits, mood, and anxiety symptoms as well as genetic vulnerability for developing the disorder; Stage I: patients who return to their baseline level of functioning when mood episodes resolve; Stage II: biomarkers and functioning impairment are related to comorbidities or rapid-…

Bipolar Disordermedia_common.quotation_subjectAnxietyModels BiologicalRisk FactorsmedicineHumansNerve Growth FactorsBipolar disorderFamily historyTemperamentBiological Psychiatrymedia_commonPharmacologyCognitive disorderCognitionmedicine.diseaseAffectMoodDisease ProgressionCytokinesAnxietyTemperamentmedicine.symptomCognition DisordersPsychologyManiaBiomarkersClinical psychologyProgress in Neuro-Psychopharmacology and Biological Psychiatry
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Persistence of the effect of birth size on dysglycaemia and type 2 diabetes in old age: AGES-Reykjavik Study

2012

We studied the effect of birth size on glucose and insulin metabolism among old non-diabetic individuals. We also explored the combined effect of birth size and midlife body mass index (BMI) on type 2 diabetes in old age. Our study comprised 1,682 Icelanders whose birth records included anthropometrical data. The same individuals had participated in the prospective population-based Reykjavik Study, where BMI was assessed at a mean age of 47 years, and in the AGES-Reykjavik Study during 2002 to 2006, where fasting glucose, insulin and HbA₁c were measured and homeostasis model assessment for the degree of insulin resistance (HOMA-IR) calculated at a mean age of 75.5 years. Type 2 diabetes was…

Blood GlucoseMaleAgingmedicine.medical_specialtyPediatricsBirth weightPopulationIcelandType 2 diabetesWeight GainArticleBody Mass IndexInsulin resistanceDiabetes mellitusInternal medicinemedicineBirth WeightHumansInsulinsyntymäpainoProspective StudieseducationAgedAged 80 and overGlucose tolerance testeducation.field_of_studydiabetesmedicine.diagnostic_testbusiness.industryIncidenceagingGeneral MedicineGlucose Tolerance TestMiddle Agedmedicine.diseaseLow birth weightikääntyminenEndocrinologyDiabetes Mellitus Type 2Population SurveillanceDisease ProgressionFemaleInsulin ResistanceGeriatrics and Gerontologymedicine.symptombusinessBody mass indexbirth sizeFollow-Up StudiesAGE
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Adiponectin, resistin and leptin in paediatric chronic renal failure: Correlation with auxological and endocrine profiles

2013

Introduction: Chronic renal failure (CRF) compromises nutrition, growth, puberty, glycometabolic homeostasis, and adipokine secretion (i.e. adiponectin, resistin, and leptin). Adipokines play a role in the clinical outcome, but data in paediatric patients is scant. Aim: To evaluate the link between kidney function, adiponectin, resistin, leptin, hormonal status, nutritional state and late outcome of CRF children. Materials and methods: We studied leptin, adiponectin and resistin levels in 31 CRF patients (19 males, 12 females, aged 12.1 ± 4.47 years) managed conservatively, and 30 healthy age- and gender-matched controls. Clinical, auxological, biochemical, hormonal data, glucose and insuli…

Blood GlucoseMaleLeptinmedicine.medical_specialtyTime FactorsAdolescentAdolescent Nutritional Physiological Phenomenamedicine.medical_treatmentNutritional StatusRenal functionAdipokineHOMA-IRchemistry.chemical_compoundSettore MED/38 - Pediatria Generale E SpecialisticaRisk FactorsInternal medicineAdipokinemedicineChronic renal failureHumansInsulinResistinObesityChildGlycated HemoglobinCreatinineAdiponectinbusiness.industryInsulinLeptinAge Factorsnutritional and metabolic diseasesPrognosismedicine.diseaseObesityEndocrinologychemistryCardiovascular DiseasesNephrologyCase-Control StudiesDisease ProgressionKidney Failure ChronicFemaleResistinAdiponectinInsulin ResistancebusinessBiomarkershormones hormone substitutes and hormone antagonists
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