Michelle H. Kim, MD, MS
she/her/hers
Instructor (Clinical)Cards
About
Research
Publications
2023
ASO Visual Abstract: The Current State of Liver Transplantation for Colorectal Liver Metastases in the United States: A Call for Standardized Reporting
Sasaki K, Ruffolo L, Kim M, Fujiki M, Hashimoto K, Imaoka Y, Melcher M, Aucejo F, Tomiyama K, Hernandez-Alejandro R. ASO Visual Abstract: The Current State of Liver Transplantation for Colorectal Liver Metastases in the United States: A Call for Standardized Reporting. Annals Of Surgical Oncology 2023, 30: 2780-2781. DOI: 10.1245/s10434-023-13234-8.Peer-Reviewed Original ResearchThe Current State of Liver Transplantation for Colorectal Liver Metastases in the United States: A Call for Standardized Reporting
Sasaki K, Ruffolo L, Kim M, Fujiki M, Hashimoto K, Imaoka Y, Melcher M, Aucejo F, Tomiyama K, Hernandez-Alejandro R. The Current State of Liver Transplantation for Colorectal Liver Metastases in the United States: A Call for Standardized Reporting. Annals Of Surgical Oncology 2023, 30: 2769-2777. PMID: 36719568, PMCID: PMC9888331, DOI: 10.1245/s10434-023-13147-6.Peer-Reviewed Original ResearchConceptsColorectal liver metastasesLiving donor LTLiver transplantationLiver metastasesNonresectable colorectal liver metastasesSurvival rateTime of LTOverall survival rateMELD-Na scoreDDLT groupLT patientsTransplant center characteristicsOncological historyDisease-freeTherapeutic optionsPatient selectionLiver tumorsHepatocellular carcinomaTransplant oncologyU.S. transplant centersPosttransplant outcomesSharing databaseTransplant centersUNOS dataPatients
2022
335.5: Has the Risk of Liver Re-Transplantation Improved Over the Two Decades? A UNOS Data Analysis
Kim M, Melcher M, Kirchner V, Gallo A, Bonham C, Esquivel C, Sasaki K. 335.5: Has the Risk of Liver Re-Transplantation Improved Over the Two Decades? A UNOS Data Analysis. Transplantation 2022, 106: s294-s294. DOI: 10.1097/01.tp.0000886948.87367.56.Peer-Reviewed Original Research
2020
Big Data in Transplantation Practice-the Devil Is in the Detail-Fontan-associated Liver Disease.
Kim M, Nguyen A, Lo M, Kumar S, Bucuvalas J, Glynn E, Hoffman M, Fischer R, Emamaullee J. Big Data in Transplantation Practice-the Devil Is in the Detail-Fontan-associated Liver Disease. Transplantation 2020, 105: 18-22. PMID: 32639398, DOI: 10.1097/tp.0000000000003308.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAge FactorsAgedAged, 80 and overBig DataChildChild, PreschoolData CollectionData MiningDatabases, FactualFemaleFontan ProcedureHeart Defects, CongenitalHumansInfantInfant, NewbornLiver DiseasesLiver TransplantationMaleMiddle AgedRisk AssessmentRisk FactorsTreatment OutcomeYoung AdultConceptsFontan-associated liver diseasePatients post-FontanPost-FontanLiver diseaseSingle-ventricle heart diseaseHeart-liver transplantationProgressive hepatic fibrosisMultiple health systemsConsequences of chronic exposureFontan procedureFontan RegistryNoncardiac complicationsHeart-liverTime of heartFontan hemodynamicsLiver transplantationHepatocellular carcinomaFontanHepatic fibrosisIndividual patientsHeart diseasePatientsHealth systemAffected childrenTransplantationLong-Term Financial, Psychosocial, and Overall Health-Related Quality of Life After Living Liver Donation
Raza M, Kim M, Ding L, Fong T, Romero C, Genyk Y, Sher L, Emamaullee J. Long-Term Financial, Psychosocial, and Overall Health-Related Quality of Life After Living Liver Donation. Journal Of Surgical Research 2020, 253: 41-52. PMID: 32320896, PMCID: PMC8351216, DOI: 10.1016/j.jss.2020.03.025.Peer-Reviewed Original ResearchConceptsHealth-related quality of lifeHealth-related qualityQuality of lifeHRQoL outcomesU.S. population normsShort Form-36Quality of Life SurveyFollow-upDiverse patient populationsPhysical activityHealthy potential donorsPopulation normsLiving liver donorsShort formHealth insuranceLifetime follow-upU.S. populationQuality of Life Survey dataLife SurveyAging populationLiver donationPatient populationPostdonation follow-upOutcomesWork performance
2019
Immunologic benefit of maternal donors in pediatric living donor liver transplantation
Kim M, Akbari O, Genyk Y, Kohli R, Emamaullee J. Immunologic benefit of maternal donors in pediatric living donor liver transplantation. Pediatric Transplantation 2019, 23: e13560. PMID: 31402535, DOI: 10.1111/petr.13560.Peer-Reviewed Original ResearchConceptsLDLT recipientsPediatric LDLT recipientsPediatric LDLTImmune tolerancePost-transplantPrimary diagnosis of biliary atresiaImpact of graft typeMechanisms of immune toleranceDiagnosis of biliary atresiaOperational toleranceImprove outcomesLong-term follow-upPediatric LDLT patientsWithdrawal of immunosuppressionRegulatory T cellsImproving allograft survivalTime post-transplantDonor liver transplantationDeceased donor recipientsMaternal-fetal microchimerismRate of rejectionLDLT patientsAllograft survivalBiliary atresiaPatient survival
2011
Myogenic Akt signaling attenuates muscular degeneration, promotes myofiber regeneration and improves muscle function in dystrophin-deficient mdx mice
Kim M, Kay D, Rudra R, Chen B, Hsu N, Izumiya Y, Martinez L, Spencer M, Walsh K, Grinnell A, Crosbie R. Myogenic Akt signaling attenuates muscular degeneration, promotes myofiber regeneration and improves muscle function in dystrophin-deficient mdx mice. Human Molecular Genetics 2011, 20: 1324-1338. PMID: 21245083, PMCID: PMC3049356, DOI: 10.1093/hmg/ddr015.Peer-Reviewed Original ResearchConceptsMdx miceMyofiber regenerationMuscular dystrophyTreatment of mdx miceDystrophin-deficient mdx miceMuscle functionEndogenous compensatory mechanismsExtensor digitorum longus muscleChildhood muscular dystrophyWild-type musclesDuchenne muscular dystrophyResponse relative to controlsGrip strength testImprove muscle functionAkt signaling pathwayDystrophin-glycoprotein complexDystrophin deficiencyOverexpression of AktExtrasynaptic sarcolemmaMuscle wastingHistopathological measurementsDystrophin geneMdxRelative to controlsMuscle degeneration
2008
Myogenic Akt signaling upregulates the utrophin–glycoprotein complex and promotes sarcolemma stability in muscular dystrophy
Peter A, Ko C, Kim M, Hsu N, Ouchi N, Rhie S, Izumiya Y, Zeng L, Walsh K, Crosbie R. Myogenic Akt signaling upregulates the utrophin–glycoprotein complex and promotes sarcolemma stability in muscular dystrophy. Human Molecular Genetics 2008, 18: 318-327. PMID: 18986978, PMCID: PMC2638781, DOI: 10.1093/hmg/ddn358.Peer-Reviewed Original ResearchConceptsMuscle wastingMuscular dystrophyAkt signalingExpression of utrophinProgressive muscle wastingDuchenne muscular dystrophyModulation of AktFunction of dystrophinSarcolemma stabilityPhysiological compensatory mechanismsDystrophin mutationsMouse modelSarcolemma damageDisease outcomeIncreased AktSarcolemma membraneDystrophyCompensatory mechanismsSignaling pathwayDystrophinSarcolemmaUtrophin-glycoprotein complexAkt
2007
Sinomenine suppresses TNF-α-induced VCAM-1 expression in human umbilical vein endothelial cells
Huang J, Lin Z, Luo M, Lu C, Kim M, Yu B, Gu J. Sinomenine suppresses TNF-α-induced VCAM-1 expression in human umbilical vein endothelial cells. Journal Of Ethnopharmacology 2007, 114: 180-185. PMID: 17869461, DOI: 10.1016/j.jep.2007.07.036.Peer-Reviewed Original ResearchMeSH KeywordsAnti-Inflammatory Agents, Non-SteroidalCell SeparationCell SurvivalCells, CulturedEndothelial CellsEndothelium, VascularFactor VIIIFlow CytometryHumansImmunohistochemistryIndicators and ReagentsMorphinansNF-kappa BReverse Transcriptase Polymerase Chain ReactionRNA, MessengerStimulation, ChemicalTumor Necrosis Factor-alphaUmbilical VeinsVascular Cell Adhesion Molecule-1ConceptsVCAM-1 expressionHuman umbilical vein endothelial cellsTNF-alpha-induced VCAM-1 expressionTNF-alphaVCAM-1 mRNA expressionVCAM-1MRNA expressionMethods of immunotherapyExpression of VCAM-1Rheumatic heart diseaseTNF-alpha-induced human umbilical vein endothelial cellsEffects in vitroUmbilical vein endothelial cellsInhibitory effect in vitroVCAM-1 mRNASymptoms of rheumatismRheumatic carditisVein endothelial cellsReal-time quantitative PCRSinomenium acutum RehdFlow cytometryHeart diseaseExperimental groupEndothelial cellsEvaluated in vitro
2006
Association of increased interferon‐inducible gene expression with disease activity and lupus nephritis in patients with systemic lupus erythematosus
Feng X, Wu H, Grossman J, Hanvivadhanakul P, FitzGerald J, Park G, Dong X, Chen W, Kim M, Weng H, Furst D, Gorn A, McMahon M, Taylor M, Brahn E, Hahn B, Tsao B. Association of increased interferon‐inducible gene expression with disease activity and lupus nephritis in patients with systemic lupus erythematosus. Arthritis & Rheumatism 2006, 54: 2951-2962. PMID: 16947629, DOI: 10.1002/art.22044.Peer-Reviewed Original ResearchConceptsSystemic lupus erythematosus patientsSystemic lupus erythematosusActive renal diseaseLupus nephritis patientsIFN scoreDisease activityLupus erythematosusNephritis patientsLupus nephritisPresence of anti-double-stranded DNARenal diseaseNormal controlsPhysician Global Assessment scoreAnti-dsDNA antibody positivityAnti-double-stranded DNAHigher IFN scoresInactive lupus nephritisSafety of EstrogensGlobal Assessment scoreAssociated with neurological manifestationsAssociated with proteinuriaLupus nephritis therapyPeripheral blood cellsRheumatic disease controlsExpression levels