2019
Prostatic Artery Embolization Using 100–300-μm Trisacryl Gelatin Microspheres to Treat Lower Urinary Tract Symptoms Attributable to Benign Prostatic Hyperplasia: A Single-Center Outcomes Analysis with Medium-Term Follow-up
Ayyagari R, Powell T, Staib L, Chapiro J, Raja A, Bhatia S, Chai T, Schoenberger S, Devito R. Prostatic Artery Embolization Using 100–300-μm Trisacryl Gelatin Microspheres to Treat Lower Urinary Tract Symptoms Attributable to Benign Prostatic Hyperplasia: A Single-Center Outcomes Analysis with Medium-Term Follow-up. Journal Of Vascular And Interventional Radiology 2019, 31: 99-107. PMID: 31771896, DOI: 10.1016/j.jvir.2019.08.005.Peer-Reviewed Original ResearchMeSH KeywordsAcrylic ResinsAge FactorsAgedAged, 80 and overComorbidityCone-Beam Computed TomographyConnecticutEmbolization, TherapeuticGelatinHumansLower Urinary Tract SymptomsMaleMiddle AgedOrgan SizeParticle SizeProstateProstatic HyperplasiaQuality of LifeRecovery of FunctionRetrospective StudiesRisk FactorsTime FactorsTreatment OutcomeConceptsInternational Prostate Symptom ScoreLower urinary tract symptomsPost-void residualCharlson Comorbidity IndexProstatic artery embolizationProstate gland volumeMedian lobe enlargementBenign prostatic hyperplasiaTrisacryl gelatin microspheresArtery embolizationProstatic hyperplasiaGland volumeAdverse event recordingMedical therapy failureClavien-Dindo classificationProstate Symptom ScoreMedium-term followUrinary tract symptomsLower urinary tractMedium-term outcomesPost-procedure valuesQuality of lifeComorbidity indexTract symptomsConsecutive patients
2018
Aspm knockout ferret reveals an evolutionary mechanism governing cerebral cortical size
Johnson MB, Sun X, Kodani A, Borges-Monroy R, Girskis KM, Ryu SC, Wang PP, Patel K, Gonzalez DM, Woo YM, Yan Z, Liang B, Smith RS, Chatterjee M, Coman D, Papademetris X, Staib LH, Hyder F, Mandeville JB, Grant PE, Im K, Kwak H, Engelhardt JF, Walsh CA, Bae BI. Aspm knockout ferret reveals an evolutionary mechanism governing cerebral cortical size. Nature 2018, 556: 370-375. PMID: 29643508, PMCID: PMC6095461, DOI: 10.1038/s41586-018-0035-0.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsBiological EvolutionCalmodulin-Binding ProteinsCentrosomeCerebral CortexDisease Models, AnimalFemaleFerretsGene DeletionGene EditingGene Expression Regulation, DevelopmentalGene Knockout TechniquesGerm-Line MutationHumansMaleMiceMicrocephalyNerve Tissue ProteinsNeural Stem CellsOrgan SizeTranscription, GeneticConceptsVentricular radial glial cellsEvolutionary mechanismsRadial glial cellsOuter radial gliaHuman primary microcephalyProtein sequence homologyAbnormal spindle-like microcephalyCerebral cortical sizeGlial cellsCortical sizeUndifferentiated cell typesNeural progenitor cellsRadial gliaASPM proteinCerebral cortical expansionMicrocephaly genesDivergent functionsGenome editingSequence homologyDifferentiated progenitorsOuter subventricular zoneCortical expansionPrimary microcephalyCell typesGermline knockout
2008
Effects of the Brain-Derived Neurotrophic Growth Factor Val66Met Variation on Hippocampus Morphology in Bipolar Disorder
Chepenik LG, Fredericks C, Papademetris X, Spencer L, Lacadie C, Wang F, Pittman B, Duncan JS, Staib LH, Duman RS, Gelernter J, Blumberg HP. Effects of the Brain-Derived Neurotrophic Growth Factor Val66Met Variation on Hippocampus Morphology in Bipolar Disorder. Neuropsychopharmacology 2008, 34: 944-951. PMID: 18704093, PMCID: PMC2837582, DOI: 10.1038/npp.2008.107.Peer-Reviewed Original ResearchConceptsSmaller hippocampus volumesHippocampus volumeBipolar disorderBDNF genotypeBD diagnosisMood disorder pathophysiologyBDNF Val66Met polymorphismHigh-resolution magnetic resonanceHealthy comparison subjectsVal/Val homozygotesEffect of diagnosisLinear mixed model analysisVal66Met polymorphismGrowth factor proteinBD subgroupsDisorder pathophysiologyHC subjectsHippocampal developmentComparison subjectsMixed model analysisHippocampus structureBDNFHippocampus morphologyAnterior hippocampusVal homozygotes