2025
The Risk and Time Course for Autoimmune Rheumatic Disease Development in Patients With Raynaud Phenomenon
Teaw S, Shojaee A, Carnaru M, Hinchcliff M. The Risk and Time Course for Autoimmune Rheumatic Disease Development in Patients With Raynaud Phenomenon. The Journal Of Rheumatology 2025, jrheum.2024-0954. PMID: 40592552, DOI: 10.3899/jrheum.2024-0954.Peer-Reviewed Original ResearchContribution of cellular immune dysregulation to myasthenia gravis pathology
Bayer A, Nowak R, O'Connor K. Contribution of cellular immune dysregulation to myasthenia gravis pathology. International Review Of Neurobiology 2025, 182: 43-66. PMID: 40675740, DOI: 10.1016/bs.irn.2025.04.035.Peer-Reviewed Original ResearchMyasthenia gravisPersistence of autoimmunityB cell compartmentAbnormal immune responseDevelopment of TResponse to treatmentCellular compartmentsImpaired neuromuscular transmissionImmunopathology of MGTolerance checkpointsComplex immunopathologyImmune dysregulationPrevent autoimmunityT cellsAutoantibody productionPathological responseAutoimmune disordersB cellsDisease developmentAutoimmune diseasesDisease progressionImmune responseMultifactorial diseaseImmune systemNeuromuscular transmission
2024
Neuroinflammation in Alzheimer disease
Heneka M, van der Flier W, Jessen F, Hoozemanns J, Thal D, Boche D, Brosseron F, Teunissen C, Zetterberg H, Jacobs A, Edison P, Ramirez A, Cruchaga C, Lambert J, Laza A, Sanchez-Mut J, Fischer A, Castro-Gomez S, Stein T, Kleineidam L, Wagner M, Neher J, Cunningham C, Singhrao S, Prinz M, Glass C, Schlachetzki J, Butovsky O, Kleemann K, De Jaeger P, Scheiblich H, Brown G, Landreth G, Moutinho M, Grutzendler J, Gomez-Nicola D, McManus R, Andreasson K, Ising C, Karabag D, Baker D, Liddelow S, Verkhratsky A, Tansey M, Monsonego A, Aigner L, Dorothée G, Nave K, Simons M, Constantin G, Rosenzweig N, Pascual A, Petzold G, Kipnis J, Venegas C, Colonna M, Walter J, Tenner A, O’Banion M, Steinert J, Feinstein D, Sastre M, Bhaskar K, Hong S, Schafer D, Golde T, Ransohoff R, Morgan D, Breitner J, Mancuso R, Riechers S. Neuroinflammation in Alzheimer disease. Nature Reviews Immunology 2024, 25: 321-352. PMID: 39653749, DOI: 10.1038/s41577-024-01104-7.Peer-Reviewed Original ResearchAlzheimer's diseasePathogenesis of Alzheimer's diseaseMultiple lines of informationGenetic studiesInfluence of geneticsLines of informationCell typesDisease developmentDementia-causing diseasesStages of Alzheimer's diseasePathological roleMultiple linesTherapeutic strategiesImmune processesPreclinical stage of Alzheimer's diseaseCellsAdaptive immune activationTargeting neuroinflammationPathological mechanismsLifestyle factorsGeneticsClinical Implications of Basic Research: Exploring the Transformative Potential of Spatial 'Omics in Uro-oncology
Figiel S, Bates A, Braun D, Eapen R, Eckstein M, Manley B, Milowsky M, Mitchell T, Bryant R, Sfakianos J, Lamb A. Clinical Implications of Basic Research: Exploring the Transformative Potential of Spatial 'Omics in Uro-oncology. European Urology 2024, 87: 8-14. PMID: 39227262, DOI: 10.1016/j.eururo.2024.08.025.Peer-Reviewed Original ResearchComputational analysis workflowMolecular dataTreatment of urological cancersGenetic changesHarmonisation of protocolsMolecular technologiesPersonalised cancer therapyCellular variationDisease developmentSpatial omicsTumor microenvironmentRisk stratificationUrological cancersCancer developmentAnalysis workflowPrecision medicineIndividual malignanciesReagent costsCancer therapyUro-oncologyCancer tissuesTumorTissue architectureClinical implicationsCancerIs Lipid Metabolism of Value in Cancer Research and Treatment? Part I- Lipid Metabolism in Cancer
Nassar A, Nie X, Zhang T, Yeung J, Norris P, He J, Ogura H, Babar M, Muldoon A, Libreros S, Chen L. Is Lipid Metabolism of Value in Cancer Research and Treatment? Part I- Lipid Metabolism in Cancer. Metabolites 2024, 14: 312. PMID: 38921447, PMCID: PMC11205345, DOI: 10.3390/metabo14060312.Peer-Reviewed Original ResearchMass spectrometryLipid metabolismTherapeutic efficacy of treatmentLipidomic studiesEfficacy of treatmentStudy of lipidsEmergence of lipidomicsLipid categoriesSpectrometryEnergy storageTumor microenvironmentPharmaceutical candidatesTherapeutic efficacyLipidomicsCancer patientsLipid profileCancer samplesCancerLarge-scale studiesCancer researchTargeted approachAlterationsDisease developmentCell growthMetabolism
2022
External validation of yonsei nomogram predicting chronic kidney disease development after partial nephrectomy: An international, multicenter study
Raheem A, Landi I, Alowidah I, Capitanio U, Montorsi F, Larcher A, Derweesh I, Ghali F, Mottrie A, Mazzone E, De Naeyer G, Campi R, Sessa F, Carini M, Minervini A, Raman J, Rjepaj C, Kriegmair M, Autorino R, Veccia A, Mir M, Claps F, Choi Y, Ham W, Santok G, Tadifa J, Syling J, Furlan M, Simeone C, Bada M, Celia A, Carrión D, Bazan A, Ruiz C, Malki M, Barber N, Hussain M, Micali S, Puliatti S, Ghaith A, Hagras A, Ghoneem A, Eissa A, Alqahtani A, Rumaih A, Alwahabi A, Alenzi M, Pavan N, Traunero F, Antonelli A, Porcaro A, Illiano E, Costantini E, Rha K. External validation of yonsei nomogram predicting chronic kidney disease development after partial nephrectomy: An international, multicenter study. International Journal Of Urology 2022, 30: 308-317. PMID: 36478459, DOI: 10.1111/iju.15108.Peer-Reviewed Original ResearchConceptsNew-onset CKDCKD stageChronic kidney disease developmentExternal validationCKD stage ICT1 renal massesKidney disease developmentPreoperative eGFRPatient ageConsecutive patientsMulticenter studyTumor sizePartial nephrectomyRenal massesProgression rateGood calibration propertiesStage IProgression probabilityPatientsNomogramIndividual riskCKDDisease developmentEGFRMedian valueTranslational opportunities of single-cell biology in atherosclerosis
de Winther M, Bäck M, Evans P, Gomez D, Goncalves I, Jørgensen H, Koenen R, Lutgens E, Norata G, Osto E, Dib L, Simons M, Stellos K, Ylä-Herttuala S, Winkels H, Bochaton-Piallat M, Monaco C. Translational opportunities of single-cell biology in atherosclerosis. European Heart Journal 2022, 44: 1216-1230. PMID: 36478058, PMCID: PMC10120164, DOI: 10.1093/eurheartj/ehac686.Peer-Reviewed Original ResearchConceptsSingle-cell biologyDisease developmentSingle-cell technologiesSingle-cell resolutionHuman biological processesSingle-cell analysisBiological processesCellular subpopulationsCardiovascular diseaseCell communityAtherosclerosis pathologyCardiovascular disease samplesTranslational opportunitiesBiologyTherapeutic strategiesInternational collaborative effortTreat diseasesField of cardiovascular diseaseClinical impactClinically relevant featuresAnalysis of atherosclerotic plaquesHiChIPdb: a comprehensive database of HiChIP regulatory interactions
Zeng W, Liu Q, Yin Q, Jiang R, Wong H. HiChIPdb: a comprehensive database of HiChIP regulatory interactions. Nucleic Acids Research 2022, 51: d159-d166. PMID: 36215037, PMCID: PMC9825415, DOI: 10.1093/nar/gkac859.Peer-Reviewed Original ResearchConceptsRegulatory interactionsChromatin conformation capture methodsCell typesArchitecture of DNADiverse cell typesComprehensive annotationGene regulationRegulatory genesHiChIPInteraction databasesRegulatory mechanismsTissue homeostasisCell differentiationFunctional interactionsComprehensive databaseCell linesDisease developmentGenesCellsCapture methodCohesinGWASH3K27acChromatinSNPsHumanized Dsp ACM Mouse Model Displays Stress-Induced Cardiac Electrical and Structural Phenotypes
Stevens TL, Manring HR, Wallace MJ, Argall A, Dew T, Papaioannou P, Antwi-Boasiako S, Xu X, Campbell SG, Akar FG, Borzok MA, Hund TJ, Mohler PJ, Koenig SN, El Refaey M. Humanized Dsp ACM Mouse Model Displays Stress-Induced Cardiac Electrical and Structural Phenotypes. Cells 2022, 11: 3049. PMID: 36231013, PMCID: PMC9562631, DOI: 10.3390/cells11193049.Peer-Reviewed Original ResearchConceptsArrhythmogenic cardiomyopathyMouse modelStructural phenotypesFibro-fatty infiltrationFirst mouse modelHeart failureChamber dilationVentricular arrhythmiasPressure overloadArrhythmic eventsCardiac performanceCardiac stressSudden deathCardiovascular stressInherited disorderG variantConnexin 43MiceDesmosomal genesReduced expressionExternal stressorsACM familyDisease developmentMurine equivalentIncomplete penetrance
2021
Exome sequencing of early-onset patients supports genetic heterogeneity in colorectal cancer
Fernández-Rozadilla C, Álvarez-Barona M, Quintana I, López-Novo A, Amigo J, Cameselle-Teijeiro J, Roman E, Gonzalez D, Llor X, Bujanda L, Bessa X, Jover R, Balaguer F, Castells A, Castellví-Bel S, Capellá G, Carracedo A, Valle L, Ruiz-Ponte C. Exome sequencing of early-onset patients supports genetic heterogeneity in colorectal cancer. Scientific Reports 2021, 11: 11135. PMID: 34045552, PMCID: PMC8159954, DOI: 10.1038/s41598-021-90590-z.Peer-Reviewed Original ResearchMeSH KeywordsAdultColorectal NeoplasmsDNA HelicasesDNA Repair EnzymesDNA-Binding ProteinsExomeExome SequencingFemaleGene Expression Regulation, NeoplasticGenetic HeterogeneityGenetic Predisposition to DiseaseHumansMaleMethyltransferasesMiddle AgedPoly-ADP-Ribose Binding ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 13ConceptsEarly-onset CRC patientsColorectal cancerCRC patientsEarly-onset patientsGenetic variantsPotential risk allelesCRC onsetYoungest caseCRC developmentIndependent patientsPatientsTruncating variantsRisk allelesExome sequencingNovel genetic variantsRobust studiesTDG geneDisease developmentCandidate variantsCancerMolecular heterogeneityDiseaseComplex diseasesGenetic heterogeneityHigh-impact variants
2020
Defining the landscape of ATP-competitive inhibitor resistance residues in protein kinases
Persky NS, Hernandez D, Do Carmo M, Brenan L, Cohen O, Kitajima S, Nayar U, Walker A, Pantel S, Lee Y, Cordova J, Sathappa M, Zhu C, Hayes TK, Ram P, Pancholi P, Mikkelsen TS, Barbie DA, Yang X, Haq R, Piccioni F, Root DE, Johannessen CM. Defining the landscape of ATP-competitive inhibitor resistance residues in protein kinases. Nature Structural & Molecular Biology 2020, 27: 92-104. PMID: 31925410, DOI: 10.1038/s41594-019-0358-z.Peer-Reviewed Original ResearchConceptsMammalian kinasesDeep mutational scanning dataDrug discovery effortsProtein kinaseMutagenesis dataMutant kinasesKinase activityDrug resistanceKinomeKinaseDiscovery effortsRelevant inhibitorsResiduesDisease developmentResistance mutationsMutationsActivation siteERK2MEK1MutantsBroader interrogationInhibitorsCSNK2A1Valuable toolTBK1
2019
ANGPTL4 in Metabolic and Cardiovascular Disease
Aryal B, Price NL, Suarez Y, Fernández-Hernando C. ANGPTL4 in Metabolic and Cardiovascular Disease. Trends In Molecular Medicine 2019, 25: 723-734. PMID: 31235370, PMCID: PMC6779329, DOI: 10.1016/j.molmed.2019.05.010.Peer-Reviewed Original ResearchConceptsCardiovascular diseaseLipoprotein lipaseRisk of atherosclerosisRole of ANGPTL4Type 2 diabetesLow-density lipoproteinFatty acidsMurine studiesPeripheral tissuesRich lipoproteinsLPL activityANGPTL4 functionsDensity lipoproteinMetabolic diseasesPossible autocrineParacrine formsDiseaseANGPTL4Disease developmentLipoproteinRecent findingsRiskTissueDifferent tissuesAtherosclerosisShort-term high-fat diet modulates several inflammatory, ER stress, and apoptosis markers in the hippocampus of young mice
Nakandakari S, Muñoz V, Kuga G, Gaspar R, Sant'Ana M, Pavan I, da Silva L, Morelli A, Simabuco F, da Silva A, de Moura L, Ropelle E, Cintra D, Pauli J. Short-term high-fat diet modulates several inflammatory, ER stress, and apoptosis markers in the hippocampus of young mice. Brain Behavior And Immunity 2019, 79: 284-293. PMID: 30797044, DOI: 10.1016/j.bbi.2019.02.016.Peer-Reviewed Original ResearchConceptsHigh-fat dietYoung miceShort-term HFD feedingMice fed high-fat dietFed high-fat dietHippocampus of miceER stressDisease developmentShort-term consumptionAlzheimer's disease developmentPotential molecular mechanismsHOMA-IRHFD feedingAD markersMicroglial cellsAD pathogenesisRisk factorsInflammatory signalsDiet modulatesΒ-amyloidCleaved caspase3HippocampusApoptosis markersHigh expressionMice
2018
Regulatory T Cells: From Discovery to Autoimmunity
Kitz A, Singer E, Hafler D. Regulatory T Cells: From Discovery to Autoimmunity. Cold Spring Harbor Perspectives In Medicine 2018, 8: a029041. PMID: 29311129, PMCID: PMC6280708, DOI: 10.1101/cshperspect.a029041.Peer-Reviewed Original ResearchConceptsAutoreactive T cellsT cellsMultiple sclerosisEffector-like T cellsInterferon γ secretionEffector T cellsRegulatory T cellsTreg cell functionT-bet expressionCentral nervous systemT cell activationFunctional TregsΓ secretionProinflammatory cytokinesVitamin DAutoimmune diseasesGenetic predispositionNervous systemLoss of functionReduced suppressionConsistent findingCell functionDisease developmentActivationCells
2017
Investigating the Impact of Maternal Residential Mobility on Identifying Critical Windows of Susceptibility to Ambient Air Pollution During Pregnancy
Warren JL, Son JY, Pereira G, Leaderer BP, Bell ML. Investigating the Impact of Maternal Residential Mobility on Identifying Critical Windows of Susceptibility to Ambient Air Pollution During Pregnancy. American Journal Of Epidemiology 2017, 187: 992-1000. PMID: 29053768, PMCID: PMC5928458, DOI: 10.1093/aje/kwx335.Peer-Reviewed Original ResearchConceptsLow birth weightTerm low birth weightMaternal residential mobilityBirth weightCritical windowBirth cohortWeekly exposurePregnancy week 16Adverse birth outcomesWindow of susceptibilityAmbient air pollutionPregnancy windowsBirth outcomesWeek 16Mother's residencePM10 exposurePregnancyResidential addressesExposure misclassificationDisease developmentCohortAir pollutionExposureAerodynamic diameterPossible mechanismOpportunities and Challenges for Environmental Exposure Assessment in Population-Based Studies
Patel C, Kerr J, Thomas D, Mukherjee B, Ritz B, Chatterjee N, Jankowska M, Madan J, Karagas M, McAllister K, Mechanic L, Fallin M, Ladd-Acosta C, Blair I, Teitelbaum S, Amos C. Opportunities and Challenges for Environmental Exposure Assessment in Population-Based Studies. Cancer Epidemiology Biomarkers & Prevention 2017, 26: 1370-1380. PMID: 28710076, PMCID: PMC5581729, DOI: 10.1158/1055-9965.epi-17-0459.Peer-Reviewed Original ResearchConceptsFollow-up of study participantsInfluence cancer riskExposure and behaviourPopulation-based studyExposure assessmentCase-control studyPhysical activityCancer riskCorrelated exposuresStudy participantsEpidemiological studiesGenetic susceptibilityEnvironmental exposure assessmentFollow-upData collectionMultidimensional indicatorsCancer developmentEvaluated 1Indicators of exposureComplex effects of environmental factorsEpidemiological investigationsOccupational exposure assessmentAssessmentEnvironmental factorsDisease developmentDo Animal Models of Acute Pancreatitis Reproduce Human Disease?
Gorelick FS, Lerch MM. Do Animal Models of Acute Pancreatitis Reproduce Human Disease? Cellular And Molecular Gastroenterology And Hepatology 2017, 4: 251-262. PMID: 28752114, PMCID: PMC5518169, DOI: 10.1016/j.jcmgh.2017.05.007.Peer-Reviewed Original ResearchAcute pancreatitisBiological disease mechanismsNonmalignant gastrointestinal diseasesPathophysiological disease mechanismsDisease mechanismsPotential therapeutic targetPaucity of dataHospital admissionCommon causeExperimental pancreatitis modelGastrointestinal diseasesPancreatitis modelTherapeutic targetAnimal modelsNatural historySpecific causesDiseaseDisease modelsPancreatitisDisease developmentUnderlying cellMolecular mechanismsHuman diseasesCauseLimited information
2016
Arg Deficiency Does not Influence the Course of Myelin Oligodendrocyte Glycoprotein (MOG35-55)-induced Experimental Autoimmune Encephalomyelitis
Jacobsen FA, Hulst C, Bäckström T, Koleske AJ, Andersson Å. Arg Deficiency Does not Influence the Course of Myelin Oligodendrocyte Glycoprotein (MOG35-55)-induced Experimental Autoimmune Encephalomyelitis. Journal Of Clinical & Cellular Immunology 2016, 2016: 420. PMID: 34527426, PMCID: PMC8439389, DOI: 10.4172/2155-9899.1000420.Peer-Reviewed Original ResearchExperimental autoimmune encephalomyelitisAutoimmune encephalomyelitisMyelin oligodendrocyte glycoproteinOligodendrocyte glycoproteinB cellsDevelopment of MOGB-cell traffickingDisease developmentSplenic B cellsLymphocyte phenotypesAbl kinaseImmune activationMultiple sclerosisImmunized miceRodent modelsEncephalomyelitisC57BL/6 backgroundStimulation assaysMiceArg kinaseNovel roleTyrosine kinaseMOGArg tyrosine kinasesActivation
2015
Nitric oxide in liver diseases
Iwakiri Y, Kim MY. Nitric oxide in liver diseases. Trends In Pharmacological Sciences 2015, 36: 524-536. PMID: 26027855, PMCID: PMC4532625, DOI: 10.1016/j.tips.2015.05.001.BooksConceptsLiver sinusoidal endothelial cellsEndothelial NO synthaseLiver diseaseNitric oxideSinusoidal endothelial cellsInducible NOSNO synthaseEndothelial cellsPathological processesDiseaseDisease developmentLiverFatty acidsS-guanylationComplicated rolePathophysiologyPathogenesisNOSProgressionImportant roleThe role of gut microbiota in the development of type 1, type 2 diabetes mellitus and obesity
Tai N, Wong FS, Wen L. The role of gut microbiota in the development of type 1, type 2 diabetes mellitus and obesity. Reviews In Endocrine And Metabolic Disorders 2015, 16: 55-65. PMID: 25619480, PMCID: PMC4348024, DOI: 10.1007/s11154-015-9309-0.Peer-Reviewed Original ResearchConceptsGut microbiotaAutoimmune type 1 diabetesType 2 diabetes mellitusInsulin-resistant type 2 diabetesMajor public health concernAltered gut microbiotaDevelopment of T1DType 2 diabetesType 1 diabetesGut microbiota compositionPublic health concernDiabetes mellitusPersistent hyperglycemiaMetabolic disordersRodent modelsMicrobiota compositionType 1ObesityDiabetesHealth concernPotential mechanismsMicrobiotaT2DT1DDisease development
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