2023
Liver Transplantation in a Woman with Mahvash Disease
Robbins J, Halegoua-DeMarzio D, Basu Mallick A, Vijayvergia N, Ganetzky R, Lavu H, Giri V, Miller J, Maley W, Shah A, DiMeglio M, Ambelil M, Yu R, Sato T, Lefler D. Liver Transplantation in a Woman with Mahvash Disease. New England Journal Of Medicine 2023, 389: 1972-1978. PMID: 37991855, DOI: 10.1056/nejmoa2303226.Peer-Reviewed Original ResearchConceptsPortal hypertensionLiver transplantationPancreatic hypertrophyMahvash diseasePancreatic α cell hyperplasiaAbsence of cirrhosisNoncirrhotic portal hypertensionΑ-cell hyperplasiaRare genetic disorderSerum glucagonDefinitive treatmentGlucagon levelsVascular diseaseMedical CenterHypertensionDiseaseAmmonia levelsHyperglucagonemiaGenetic disordersTransplantationHypertrophyGlucagonWomenHematemesisCirrhosis
2022
Transurethral resection of posterior urethral valves
Arlen A. Transurethral resection of posterior urethral valves. Urology Video Journal 2022, 15: 100165. DOI: 10.1016/j.urolvj.2022.100165.Peer-Reviewed Original ResearchPosterior urethral valvesUrethral valvesVesicoureteral refluxLower urinary tract obstructionBladder neck hypertrophyBladder wall thickeningUpper tract dilationStage renal diseaseUrinary tract obstructionFetal development resultsTract obstructionRenal diseaseTransurethral resectionDetrusor hypertrophyTract dilationPosterior urethraCommon causeWall thickeningMost valvesHypertrophyDilationValveResectionUrethraObstructionImproving detection of cerebral small vessel disease aetiology in patients with isolated lobar intracerebral haemorrhage
Das A, Gokcal E, Regenhardt R, Horn M, Schwab K, Daoud N, Viswanathan A, Kimberly W, Goldstein J, Biffi A, Rost N, Rosand J, Schwamm L, Greenberg S, Gurol M. Improving detection of cerebral small vessel disease aetiology in patients with isolated lobar intracerebral haemorrhage. Stroke And Vascular Neurology 2022, 8: 26-33. PMID: 35981809, PMCID: PMC9985798, DOI: 10.1136/svn-2022-001653.Peer-Reviewed Original ResearchConceptsLeft ventricular hypertrophyCerebral amyloid angiopathyLobar intracerebral hemorrhageIntracerebral hemorrhageImaging markerFrequency of LVHCerebral small vessel diseaseSmall vessel diseaseAetiologic groupsLobar lacunesAmyloid angiopathyVentricular hypertrophyVessel diseasePresence/distributionPatientsDisease etiologyHemorrhageLacunesMarkersRegression modelsAngiopathyHigh frequencyHypertrophyEtiologyDiseaseLung Injury Induces Alveolar Type 2 Cell Hypertrophy and Polyploidy with Implications for Repair and Regeneration.
Weng A, Maciel Herrerias M, Watanabe S, Welch LC, Flozak AS, Grant RA, Aillon RP, Dada LA, Han SH, Hinchcliff M, Misharin AV, Budinger GRS, Gottardi CJ. Lung Injury Induces Alveolar Type 2 Cell Hypertrophy and Polyploidy with Implications for Repair and Regeneration. American Journal Of Respiratory Cell And Molecular Biology 2022, 66: 564-576. PMID: 35202558, PMCID: PMC9116356, DOI: 10.1165/rcmb.2021-0356oc.Peer-Reviewed Original ResearchConceptsLung injuryCell hypertrophyAT2 cellsAlveolar epithelial injuryIntegrated stress responseDistal lung epitheliumBleomycin injuryEpithelial injuryLung epitheliumInjuryBarrier restorationHypertrophic growthSmall molecule ISRIBWound healingFacultative progenitorsHypertrophyStress responseAT2BinucleationCellsReinjuryShort termEpitheliumResponse
2021
Loss of crossbridge inhibition drives pathological cardiac hypertrophy in patients harboring the TPM1 E192K mutation
Sewanan LR, Park J, Rynkiewicz MJ, Racca AW, Papoutsidakis N, Schwan J, Jacoby DL, Moore JR, Lehman W, Qyang Y, Campbell SG. Loss of crossbridge inhibition drives pathological cardiac hypertrophy in patients harboring the TPM1 E192K mutation. Journal Of General Physiology 2021, 153: e202012640. PMID: 34319370, PMCID: PMC8321830, DOI: 10.1085/jgp.202012640.Peer-Reviewed Original ResearchConceptsHypertrophic cardiomyopathyHeart tissueCellular hypertrophyEngineered Heart TissuePathological cardiac hypertrophyThin filament mutationsMavacamten treatmentDiastolic dysfunctionDisease featuresHypertrophic effectCardiac hypertrophyContractile differencesHypertrophyFundamental disease mechanismsCrossbridge activityInherited disorderOverall Ca2Uncertain significancePatient phenotypesDisease mechanismsLow Ca2PatientsK mutationMavacamtenTissue197-LB: The Regulation of HSL by Macrophage Migration Inhibitory Factor (MIF) Contributes to Adipocyte Hypertrophy and Development of Obesity
CHEN L, HUANG Y, LI L, ZABIHI H, QI Y, LENG L, SUN G, BUCALA R, QI D. 197-LB: The Regulation of HSL by Macrophage Migration Inhibitory Factor (MIF) Contributes to Adipocyte Hypertrophy and Development of Obesity. Diabetes 2021, 70 DOI: 10.2337/db21-197-lb.Peer-Reviewed Original ResearchRight Ventricular Fatty Infiltration With an Abnormal ECG
Odanovic N, Mojibian HR, Young LH. Right Ventricular Fatty Infiltration With an Abnormal ECG. JACC Case Reports 2021, 3: 314-318. PMID: 34317526, PMCID: PMC8310990, DOI: 10.1016/j.jaccas.2020.11.017.Peer-Reviewed Case Reports and Technical NotesFatty infiltrationCardiac magnetic resonance imagingArrhythmogenic right ventricular cardiomyopathyRight ventricular hypertrophyBenign clinical courseRight ventricular cardiomyopathyMiddle-aged womenMagnetic resonance imagingClinical courseVentricular hypertrophyVentricular thickeningRoutine electrocardiogramVentricular cardiomyopathyAbnormal ECGResonance imagingInfiltrationEchocardiogramPatientsCardiomyopathyHypertrophyElectrocardiogramWomen
2019
P4429Cardiac magnetic resonance characteristics of professional athletes and hypertrophic cardiomyopathy patients in the grey zone of hypertrophy
Czimbalmos C, Csecs I, Dohy Z, Toth A, Suhai F, Szabo L, Horvath V, Sydo N, Kiss O, Becker D, Merkely B, Vago H. P4429Cardiac magnetic resonance characteristics of professional athletes and hypertrophic cardiomyopathy patients in the grey zone of hypertrophy. European Heart Journal 2019, 40: ehz745.0831. DOI: 10.1093/eurheartj/ehz745.0831.Peer-Reviewed Original ResearchMale HCM patientsHCM patientsHypertrophic cardiomyopathy patientsHypertrophic cardiomyopathyHealthy athletesEjection fractionLeft ventricular (LV) ejection fractionLV) ejection fractionConventional CMR parametersCardiac magnetic resonanceEnd-diastolic wall thicknessLV hypertrophyCardiomyopathy patientsNo significant differenceCMR parametersGray zoneHCM groupEnd-diastolicPhysiological hypertrophyPatient groupAthlete's heartEnd-systolePatientsHypertrophyStroke volumeExtrahepatic Clinical Application of Vessel Tracking Software and 3D Roadmapping Tools: Preliminary Experience
Sundararajan SH, McClure TD, Winokur RS, Kishore SA, Madoff DC. Extrahepatic Clinical Application of Vessel Tracking Software and 3D Roadmapping Tools: Preliminary Experience. Journal Of Vascular And Interventional Radiology 2019, 30: 1021-1026. PMID: 31003843, DOI: 10.1016/j.jvir.2018.11.039.Peer-Reviewed Original ResearchMeSH KeywordsAgedAneurysm, FalseCarcinoma, Renal CellComputed Tomography AngiographyEmbolization, TherapeuticFemaleGastrointestinal HemorrhageHumansImaging, Three-DimensionalKidney NeoplasmsMaleMesenteric Artery, SuperiorPancreaticoduodenectomyPostoperative HemorrhagePredictive Value of TestsPreliminary DataProstateProstatic HyperplasiaRadiographic Image Interpretation, Computer-AssistedRadiography, InterventionalRenal ArteryRetrospective StudiesSoftwareTreatment OutcomeThe demanding grey zone: Sport indices by cardiac magnetic resonance imaging differentiate hypertrophic cardiomyopathy from athlete’s heart
Czimbalmos C, Csecs I, Toth A, Kiss O, Suhai F, Sydo N, Dohy Z, Apor A, Merkely B, Vago H. The demanding grey zone: Sport indices by cardiac magnetic resonance imaging differentiate hypertrophic cardiomyopathy from athlete’s heart. PLOS ONE 2019, 14: e0211624. PMID: 30763323, PMCID: PMC6375568, DOI: 10.1371/journal.pone.0211624.Peer-Reviewed Original ResearchConceptsCardiac magnetic resonancePathological left ventricular hypertrophyHypertrophic cardiomyopathyVentricular hypertrophySport indexCardiac magnetic resonance imagingEnd-diastolic volume ratioHypertrophic cardiomyopathy patientsLeft ventricular massEnd-diastolic wall thicknessCut-off valueGray zoneMagnetic resonance imagingHCM patientsCardiomyopathy patientsTrained athletesVentricular massPhysiological hypertrophyDiagnostic accuracyAthlete's heartCardiomyopathyHypertrophyMale subgroupResonance imagingEDWT
2018
Cardiomyocyte gene programs encoding morphological and functional signatures in cardiac hypertrophy and failure
Nomura S, Satoh M, Fujita T, Higo T, Sumida T, Ko T, Yamaguchi T, Tobita T, Naito AT, Ito M, Fujita K, Harada M, Toko H, Kobayashi Y, Ito K, Takimoto E, Akazawa H, Morita H, Aburatani H, Komuro I. Cardiomyocyte gene programs encoding morphological and functional signatures in cardiac hypertrophy and failure. Nature Communications 2018, 9: 4435. PMID: 30375404, PMCID: PMC6207673, DOI: 10.1038/s41467-018-06639-7.Peer-Reviewed Original ResearchConceptsCardiac hypertrophyCardiomyocyte remodelingGene programHeart failurePressure overloadMorphological hypertrophyHeart functionHypertrophyP53 deletionEarly hypertrophyFunctional signaturesFunctional phenotypeLate hypertrophyP53 signalingTranscriptional signatureProgram activationMitochondrial inhibitionUnderlying mechanismCardiomyocyte identityCardiomyocytesMitochondrial activationRemodelingFailureTranscriptional programsActivationCardiac Hypertrophy: Signaling and Cellular Crosstalk
Tirziu D. Cardiac Hypertrophy: Signaling and Cellular Crosstalk. 2018 DOI: 10.1016/b978-0-12-801238-3.99834-9.Peer-Reviewed Original ResearchCardiac hypertrophyHypertrophic responseHemodynamic stressMolecular basisPathological hypertrophic responsesCellular crosstalkVariety of stimuliMyocardial infarctionImmune cellsCardiac performanceHypertrophic growthChronic increaseVascular cellsPhysiological stimuliCellular communicationMajor playersCardiac cellsWall stressHypertrophyCellsCrosstalkCardiomyocytesPrimary mechanismSignalingStressCardiac Hypertrophy: Signaling and Cellular Crosstalk
Tirziu D. Cardiac Hypertrophy: Signaling and Cellular Crosstalk. 2018, 434-450. DOI: 10.1016/b978-0-12-809657-4.99834-x.Peer-Reviewed Original ResearchCardiac hypertrophyHypertrophic responseHemodynamic stressMolecular basisPathological hypertrophic responsesCellular crosstalkVariety of stimuliMyocardial infarctionImmune cellsCardiac performanceHypertrophic growthChronic increaseVascular cellsPhysiological stimuliCellular communicationMajor playersCardiac cellsWall stressHypertrophyCellsCrosstalkCardiomyocytesPrimary mechanismSignalingStress
2017
Urinary bladder hypertrophy characteristic of male ROMK Bartter’s mice does not occur in female mice
Kim JM, Xu S, Guo X, Hu H, Dong K, Wang T. Urinary bladder hypertrophy characteristic of male ROMK Bartter’s mice does not occur in female mice. AJP Regulatory Integrative And Comparative Physiology 2017, 314: r334-r341. PMID: 29092859, PMCID: PMC5899254, DOI: 10.1152/ajpregu.00315.2017.Peer-Reviewed Original ResearchConceptsKO miceBladder hypertrophyBladder weightUrinary bladder hypertrophyRenal outer medullary potassium channelSeverity of hydronephrosisWild-type miceROMK knockout miceBladder capacityDetrusor muscleWT miceUrinary tractBartter's syndromeFemale miceSalt wastingHydronephrosisKnockout miceROMK expressionMiceBladderHypertrophyPotassium channelsMRNA levelsSignificant enlargementSyndrome
2016
Normalizing translation through 4E-BP prevents mTOR-driven cortical mislamination and ameliorates aberrant neuron integration
Lin TV, Hsieh L, Kimura T, Malone TJ, Bordey A. Normalizing translation through 4E-BP prevents mTOR-driven cortical mislamination and ameliorates aberrant neuron integration. Proceedings Of The National Academy Of Sciences Of The United States Of America 2016, 113: 11330-11335. PMID: 27647922, PMCID: PMC5056085, DOI: 10.1073/pnas.1605740113.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsCarrier ProteinsCell Cycle ProteinsDendritic SpinesEukaryotic Initiation FactorsExcitatory Postsynaptic PotentialsGene Knockdown TechniquesGreen Fluorescent ProteinsMatrix Attachment Region Binding ProteinsMechanistic Target of Rapamycin Complex 1MiceNeurogliaNeuronsPhosphoproteinsProtein BiosynthesisRas Homolog Enriched in Brain ProteinRNA CapsRNA, Small InterferingSignal TransductionTOR Serine-Threonine KinasesTranscription FactorsConceptsBrain cytoarchitectureUpper layer cortical neuronsHyperactive mammalian targetDendritic hypertrophyCortical neuronsCap-dependent translationEctopic placementRadial gliaMammalian targetLate corticogenesisTranslational repressor eukaryotic initiation factor 4EEukaryotic initiation factor 4ENeurodevelopmental disordersProtein 1Rapamycin complex 1Molecular hallmarksInitiation factor 4EMechanisms downstreamCytoarchitectureMolecular identityMisplacementActive mutantHypertrophyGliaOveractivationEndothelial Nogo-B regulates sphingolipid biosynthesis to promote the transition from hypertrophy to heart failure during chronic pressure overload
Zhang Y, Huang Y, Cantalupo A, Azevedo P, Siragusa M, Giordano F, Di Lorenzo A. Endothelial Nogo-B regulates sphingolipid biosynthesis to promote the transition from hypertrophy to heart failure during chronic pressure overload. International Journal Of Cardiology Cardiovascular Risk And Prevention 2016, 10: e2. DOI: 10.1016/j.jash.2016.03.006.Peer-Reviewed Original ResearchmiR-182 Modulates Myocardial Hypertrophic Response Induced by Angiogenesis in Heart
Li N, Hwangbo C, Jaba IM, Zhang J, Papangeli I, Han J, Mikush N, Larrivée B, Eichmann A, Chun HJ, Young LH, Tirziu D. miR-182 Modulates Myocardial Hypertrophic Response Induced by Angiogenesis in Heart. Scientific Reports 2016, 6: 21228. PMID: 26888314, PMCID: PMC4758045, DOI: 10.1038/srep21228.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCardiomegalyEndotheliumMechanistic Target of Rapamycin Complex 1Membrane ProteinsMiceMice, KnockoutMicroRNAsMultiprotein ComplexesMyocytes, CardiacNeovascularization, PathologicNitric OxideNitric Oxide Synthase Type IIIProteinsProto-Oncogene Proteins c-aktRGS ProteinsTOR Serine-Threonine KinasesUp-RegulationConceptsHypertrophic responseMiR-182Myocardial hypertrophyEndothelial-cardiomyocyte crosstalkLV pressure overloadEndothelium-derived NOPlacental growth factorMyocardial hypertrophic responseDevelopment of hypertrophyDegradation of regulatorsMiR-182 targetsHemodynamic demandsPressure overloadPlGF expressionBlood supplyParacrine actionCardiomyocyte hypertrophyMyocardial angiogenesisCardiac angiogenesisTreatment inhibitsHypertrophyAKT/mTORC1 pathwaysNovel targetAkt/Growth factor
2015
AMPK deficiency in cardiac muscle results in dilated cardiomyopathy in the absence of changes in energy metabolism
Sung MM, Zordoky BN, Bujak AL, Lally JS, Fung D, Young ME, Horman S, Miller EJ, Light PE, Kemp BE, Steinberg GR, Dyck JR. AMPK deficiency in cardiac muscle results in dilated cardiomyopathy in the absence of changes in energy metabolism. Cardiovascular Research 2015, 107: 235-245. PMID: 26023060, PMCID: PMC4565988, DOI: 10.1093/cvr/cvv166.Peer-Reviewed Original ResearchConceptsHeart failureCardiac functionCardiac hypertrophyRole of AMPKAMPK deficiencyCompensatory cardiac hypertrophyWild-type littermatesFatty acid oxidation ratesMyocardial energy metabolismAlters cardiac functionMuscle-specific deletionFirst mouse modelDiastolic functionAbsence of changesCardiac dysfunctionWT miceBasal glucoseMyocardial functionMyocardial metabolismCell shorteningMouse modelCardiac muscle resultsHypertrophyImpaired activationTroponin I
2014
Early life stress and macaque amygdala hypertrophy: preliminary evidence for a role for the serotonin transporter gene
Coplan JD, Fathy HM, Jackowski AP, Tang CY, Perera TD, Mathew SJ, Martinez J, Abdallah CG, Dwork AJ, Pantol G, Carpenter D, Gorman JM, Nemeroff CB, Owens MJ, Kaffman A, Kaufman J. Early life stress and macaque amygdala hypertrophy: preliminary evidence for a role for the serotonin transporter gene. Frontiers In Behavioral Neuroscience 2014, 8: 342. PMID: 25339875, PMCID: PMC4186477, DOI: 10.3389/fnbeh.2014.00342.Peer-Reviewed Original ResearchLarger amygdala volumesAmygdala volumeSerotonin transporter geneFractional anisotropyCerebrospinal fluid concentrationsEarly life stressRight amygdala volumeAnxiety-like responsesHippocampal neurogenesisInternal capsuleAnterior limbMRI scansLeft amygdalaSecondary analysisFluid concentrationsYoung adulthoodTransporter geneLife stressNeurobiological parametersPersistent changesHypertrophyPreliminary evidenceShort alleleAdulthoodStress-related variablesPlasma Cardiotrophin‐1 Levels are Associated With Hypertensive Heart Disease: A Meta‐Analysis
Song K, Wang S, Huang B, Luciano A, Srivastava R, Mani A. Plasma Cardiotrophin‐1 Levels are Associated With Hypertensive Heart Disease: A Meta‐Analysis. Journal Of Clinical Hypertension 2014, 16: 686-692. PMID: 25052897, PMCID: PMC4159421, DOI: 10.1111/jch.12376.Peer-Reviewed Original ResearchConceptsCT-1 levelsPlasma CT-1 levelsHypertensive heart diseaseHeart failureLeft ventricular hypertrophyVentricular hypertrophyCardiotrophin-1Hypertensive patientsHeart diseaseHypertension-induced left ventricular hypertrophyCardiotrophin-1 levelsSmall independent studiesHypertension-induced hypertrophyInterleukin-6 cytokineNormotensive patientsSerum levelsSubgroup analysisCardiac hypertrophyNovel biomarkersHypertensionPatientsElectronic databasesHypertrophyMeta-analysisStandardized algorithm
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