2022
Type IV Pili Are a Critical Virulence Factor in Clinical Isolates of Paenibacillus thiaminolyticus
Hehnly C, Shi A, Ssentongo P, Zhang L, Isaacs A, Morton S, Streck N, Erdmann-Gilmore P, Tolstoy I, Townsend R, Limbrick D, Paulson J, Ericson J, Galperin M, Schiff S, Broach J. Type IV Pili Are a Critical Virulence Factor in Clinical Isolates of Paenibacillus thiaminolyticus. MBio 2022, 13: e02688-22. PMID: 36374038, PMCID: PMC9765702, DOI: 10.1128/mbio.02688-22.Peer-Reviewed Original ResearchConceptsPostinfectious hydrocephalusClinical isolatesVirulence factorsCritical virulence factorPotential virulence factorsPoor long-term outcomesPrevention of hydrocephalusLong-term outcomesBacterial pathogensDevastating sequelaeNeonatal sepsisMiddle-income countriesNeonatal infectionSurgical interventionReference strainsNovel bacterial pathogensAfrican cohortBeta-lactamase genesChildhood mortalityHydrocephalusTherapeutic targetInfectionVirulent strainDevastating diseaseWhole-genome sequencing
2021
TET2 Protects Against Vascular Smooth Muscle Cell Apoptosis and Intimal Thickening in Transplant Vasculopathy
Ostriker AC, Xie Y, Chakraborty R, Sizer AJ, Bai Y, Ding M, Song WL, Huttner A, Hwa J, Martin KA. TET2 Protects Against Vascular Smooth Muscle Cell Apoptosis and Intimal Thickening in Transplant Vasculopathy. Circulation 2021, 144: 455-470. PMID: 34111946, PMCID: PMC8643133, DOI: 10.1161/circulationaha.120.050553.Peer-Reviewed Original ResearchMeSH KeywordsAllograftsAnimalsApoptosisBiomarkersDioxygenasesDisease Models, AnimalDisease SusceptibilityDNA-Binding ProteinsHeart TransplantationHumansImmunohistochemistryInterferon-gammaMiceMice, KnockoutMyocytes, Smooth MuscleSignal TransductionSTAT1 Transcription FactorTunica IntimaVascular DiseasesConceptsCoronary allograft vasculopathyGraft arteriopathyIntimal thickeningCAV progressionRole of TET2VSMC apoptosisTransplant samplesGraft modelHigh-dose ascorbic acidTET2 expressionVSMC phenotypeContext of transplantCoronary blood flowEffect of IFNγTET2 activityTET2 depletionSmooth muscle cell apoptosisVascular smooth muscle cell apoptosisMuscle cell apoptosisAllograft vasculopathyDevastating sequelaeMedial thinningAortic graftHeart transplantTransplant failure
2020
Paradoxical aortic stiffening and subsequent cardiac dysfunction in Hutchinson–Gilford progeria syndrome
Murtada SI, Kawamura Y, Caulk AW, Ahmadzadeh H, Mikush N, Zimmerman K, Kavanagh D, Weiss D, Latorre M, Zhuang ZW, Shadel GS, Braddock DT, Humphrey JD. Paradoxical aortic stiffening and subsequent cardiac dysfunction in Hutchinson–Gilford progeria syndrome. Journal Of The Royal Society Interface 2020, 17: 20200066. PMID: 32453981, PMCID: PMC7276555, DOI: 10.1098/rsif.2020.0066.Peer-Reviewed Original ResearchConceptsHutchinson-Gilford progeria syndromeSubsequent cardiac dysfunctionSmooth muscle functionPulse wave velocityUltra-rare disordersCardiovascular eventsDevastating sequelaeDiastolic dysfunctionSystolic functionCardiac dysfunctionProgeria syndromeVascular functionAortic functionMuscle functionEarly deathMouse modelTherapeutic windowCardiovascular dataBiomechanical phenotypingDysfunctionSyndromeExcessive accumulationBiomechanical functionArterial developmentPressure-related effects
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