2024
Adjunctive Intravenous Argatroban or Eptifibatide for Ischemic Stroke
Adeoye O, Broderick J, Derdeyn C, Grotta J, Barsan W, Bentho O, Berry S, Concha M, Davis I, Demel S, Elm J, Gentile N, Graves T, Hoffman M, Huang J, Ingles J, Janis S, Jasne A, Khatri P, Levine S, Majjhoo A, Panagos P, Pancioli A, Pizzella S, Ranasinghe T, Sabagha N, Sivakumar S, Streib C, Vagal A, Wilson A, Wintermark M, Yoo A, Barreto A. Adjunctive Intravenous Argatroban or Eptifibatide for Ischemic Stroke. New England Journal Of Medicine 2024, 391: 810-820. PMID: 39231343, PMCID: PMC11528349, DOI: 10.1056/nejmoa2314779.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnticoagulantsArginineCombined Modality TherapyDrug Therapy, CombinationEptifibatideFemaleFibrinolytic AgentsHumansIncidenceInfusions, IntravenousIntracranial HemorrhagesIschemic StrokeMaleMiddle AgedPeptidesPipecolic AcidsPlatelet Aggregation InhibitorsSingle-Blind MethodSulfonamidesThrombectomyThrombolytic TherapyTreatment OutcomeConceptsSymptomatic intracranial hemorrhageIntravenous argatrobanIntravenous thrombolysisAcute ischemic strokeIntracranial hemorrhageIschemic strokeIncidence of symptomatic intracranial hemorrhageSymptom onsetIschemic stroke treated with intravenous thrombolysisAcute ischemic stroke treated with intravenous thrombolysisStroke treated with intravenous thrombolysisAssociated with increased mortalityRankin Scale scoreInitiation of thrombolysisControlled clinical trialsTreatment of acute ischemic strokePlacebo groupEptifibatide groupEfficacy outcomesArgatroban groupStandard treatmentAdjunctive treatmentPlaceboClinical trialsArgatrobanStructural study for substrate recognition of human N‐terminal glutamine amidohydrolase 1 in the arginine N‐degron pathway
Kang J, Park J, Lee J, Jang J, Han B. Structural study for substrate recognition of human N‐terminal glutamine amidohydrolase 1 in the arginine N‐degron pathway. Protein Science 2024, 33: e5067. PMID: 38864716, PMCID: PMC11168063, DOI: 10.1002/pro.5067.Peer-Reviewed Original ResearchConceptsN-degron pathwaySubstrate recognitionN-degronSubstrate-binding conformationHalf-life of proteinsProtein degradation machineryTargeted protein therapyDegradation machinerySubstrate specificityProtein regulationBackbone of proteinsGln residuesCharged residuesNT residuesDegradation systemProteinBiochemical analysisResiduesPathwayStructural studiesGlnProtein therapyArginineSide chainsShed light
2023
Lysine Demethylation in Pathogenesis
Cao J, Yan Q. Lysine Demethylation in Pathogenesis. Advances In Experimental Medicine And Biology 2023, 1433: 1-14. PMID: 37751133, DOI: 10.1007/978-3-031-38176-8_1.ChaptersConceptsLysine demethylasesLSD1/KDM1AHistone lysine methylationHistone lysine methyltransferasesMajor epigenetic mechanismsNormal developmentNon-histone substratesSpecific small molecule inhibitorsSmall molecule inhibitorsLysine methylationLysine methyltransferasesHistone methylationHistone lysineLysine demethylationEpigenetic mechanismsDNA repairArginine residuesHuman diseasesMore subfamiliesMolecule inhibitorsLysine modificationDemethylasesMethylationTreatment of cancerEnzymeSickle Cell Disease Treatment with Arginine Therapy (STArT): study protocol for a phase 3 randomized controlled trial
Rees C, Brousseau D, Cohen D, Villella A, Dampier C, Brown K, Campbell A, Chumpitazi C, Airewele G, Chang T, Denton C, Ellison A, Thompson A, Ahmad F, Bakshi N, Coleman K, Leibovich S, Leake D, Hatabah D, Wilkinson H, Robinson M, Casper T, Vichinsky E, Morris C. Sickle Cell Disease Treatment with Arginine Therapy (STArT): study protocol for a phase 3 randomized controlled trial. Trials 2023, 24: 538. PMID: 37587492, PMCID: PMC10433602, DOI: 10.1186/s13063-023-07538-z.Peer-Reviewed Original ResearchConceptsPediatric Emergency Care Applied Research NetworkSickle cell disease treatmentVaso-occlusive episodesSickle cell diseaseSTART trialArginine therapyIntravenous arginineLoading doseNormal saline three timesYoung adultsBlood Institute guidelinesParental opioid usePlacebo loading doseSubstantial illness burdenDisease-modifying therapiesPatient-reported outcomesDisease treatmentPhase 3Emergency medicine providersSaline three timesMulticenter research networkResearch NetworkIntravenous opioidsLast doseStudy drug
2022
Transcriptome of Epibiont Saccharibacteria Nanosynbacter lyticus Strain TM7x During the Establishment of Symbiosis
Hendrickson EL, Bor B, Kerns KA, Lamont EI, Chang Y, Liu J, Cen L, Schulte F, Hardt M, Shi W, He X, McLean JS. Transcriptome of Epibiont Saccharibacteria Nanosynbacter lyticus Strain TM7x During the Establishment of Symbiosis. Journal Of Bacteriology 2022, 204: e00112-22. PMID: 35975994, PMCID: PMC9487520, DOI: 10.1128/jb.00112-22.Peer-Reviewed Original ResearchConceptsCandidate Phyla RadiationEstablishment of symbiosisStable symbiosisStress-related genesGene expressionReduced genomePeptidoglycan biosynthesisHost bacteriaHuman microbiomeBiosynthesis gene expressionMonophyletic radiationCell sizeEffector genesPartitioning genesObligate parasitesUnique organismsBiosynthetic pathwayHigher gene expressionCell shapeTransporter geneCell wallObligate epibiontsLow expressionSymbiosisCell cycle
2021
Safety of intravenous arginine therapy in children with sickle cell disease hospitalized for vaso‐occlusive pain: A randomized placebo‐controlled trial in progress
Reyes L, Figueroa J, Leake D, Khemani K, Kumari P, Bakshi N, Lane P, Dampier C, Morris C. Safety of intravenous arginine therapy in children with sickle cell disease hospitalized for vaso‐occlusive pain: A randomized placebo‐controlled trial in progress. American Journal Of Hematology 2021, 97: e21-e24. PMID: 34724240, PMCID: PMC8722015, DOI: 10.1002/ajh.26396.Peer-Reviewed Original ResearchMethylation of dual-specificity phosphatase 4 controls cell differentiation
Su H, Jiang M, Senevirathne C, Aluri S, Zhang T, Guo H, Xavier-Ferrucio J, Jin S, Tran NT, Liu SM, Sun CW, Zhu Y, Zhao Q, Chen Y, Cable L, Shen Y, Liu J, Qu CK, Han X, Klug CA, Bhatia R, Chen Y, Nimer SD, Zheng YG, Iancu-Rubin C, Jin J, Deng H, Krause DS, Xiang J, Verma A, Luo M, Zhao X. Methylation of dual-specificity phosphatase 4 controls cell differentiation. Cell Reports 2021, 36: 109421. PMID: 34320342, PMCID: PMC9110119, DOI: 10.1016/j.celrep.2021.109421.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnimalsArginineCell DifferentiationCell LineChildDual-Specificity PhosphatasesEnzyme StabilityFemaleHEK293 CellsHumansMaleMAP Kinase Signaling SystemMegakaryocytesMethylationMice, Inbred C57BLMiddle AgedMitogen-Activated Protein Kinase PhosphatasesMyelodysplastic Syndromesp38 Mitogen-Activated Protein KinasesPolyubiquitinProtein-Arginine N-MethyltransferasesProteolysisRepressor ProteinsUbiquitinationYoung AdultConceptsDual-specificity phosphataseCell differentiationSingle-cell transcriptional analysisP38 MAPKControls cell differentiationE3 ligase HUWE1Knockdown screeningMK differentiationTranscriptional analysisMegakaryocyte differentiationProtein kinaseP38 axisP38 activationPRMT1Transcriptional signatureContext of thrombocytopeniaMK cellsMechanistic insightsPharmacological inhibitionDifferentiationMethylationMAPKPhosphataseUbiquitinylationActivationDMA-tudor interaction modules control the specificity of in vivo condensates
Courchaine EM, Barentine AES, Straube K, Lee DR, Bewersdorf J, Neugebauer KM. DMA-tudor interaction modules control the specificity of in vivo condensates. Cell 2021, 184: 3612-3625.e17. PMID: 34115980, PMCID: PMC8402948, DOI: 10.1016/j.cell.2021.05.008.Peer-Reviewed Original ResearchTopical arginase inhibition decreases growth of cutaneous squamous cell carcinoma
Mittal A, Wang M, Vidyarthi A, Yanez D, Pizzurro G, Thakral D, Tracy E, Colegio OR. Topical arginase inhibition decreases growth of cutaneous squamous cell carcinoma. Scientific Reports 2021, 11: 10731. PMID: 34031449, PMCID: PMC8144401, DOI: 10.1038/s41598-021-90200-y.Peer-Reviewed Original ResearchConceptsCutaneous squamous cell carcinomaSquamous cell carcinomaArginase inhibitionB6 miceCell carcinomaAnti-PD-1 therapeutic efficacyTumor growthArginase inhibitorAnti-PD-1 therapyPD-1 expressionAppropriate tumor modelsCSCC cell linesPre-clinical modelsTumor growth inhibitionNOHA administrationSignificant morbidityC57BL/6 miceImmune microenvironmentImmunocompetent miceCSCC tumorsDeficient miceT cellsMacrophage expressionTherapeutic modalitiesTherapeutic efficacyThe Dimethylarginines (Asymmetric and Symmetric): A Deadly Combination in Sepsis
El-Khoury JM. The Dimethylarginines (Asymmetric and Symmetric): A Deadly Combination in Sepsis. The Journal Of Applied Laboratory Medicine 2021, 6: 577-579. PMID: 33544823, DOI: 10.1093/jalm/jfaa241.Peer-Reviewed Original Research
2020
Penicillin G Induces H+, K+-ATPase via a Nitric Oxide-Dependent Mechanism in the Rat Colonic Crypt
Baratta VM, Norz V, Barahona MJ, Gisinger TM, Mulligan D, Geibel JP. Penicillin G Induces H+, K+-ATPase via a Nitric Oxide-Dependent Mechanism in the Rat Colonic Crypt. Cellular Physiology And Biochemistry 2020, 54: 1132-1142. PMID: 33175479, PMCID: PMC8095381, DOI: 10.33594/000000305.Peer-Reviewed Original ResearchConceptsRat colonic cryptsColonic cryptsNitric oxideNitric oxide-dependent mechanismPotassium homeostasisArginine methyl esterAmmonium prepulse techniqueIntracellular nitric oxideSodium-free conditionsL-NAMEDiarrheal statesATPase activityBACKGROUND/Presence of NOPenicillin G sodium saltAcute exposureL-arginineSmall intestineIsolated administrationN-nitroHomeostatic conditionsCryptsPrepulse techniqueSignificant reductionNovel mechanism
2018
An Invariant Arginine in Common with MHC Class II Allows Extension at the C-Terminal End of Peptides Bound to Chicken MHC Class I
Xiao J, Xiang W, Zhang Y, Peng W, Zhao M, Niu L, Chai Y, Qi J, Wang F, Qi P, Pan C, Han L, Wang M, Kaufman J, Gao G, Liu W. An Invariant Arginine in Common with MHC Class II Allows Extension at the C-Terminal End of Peptides Bound to Chicken MHC Class I. The Journal Of Immunology 2018, 201: 3084-3095. PMID: 30341185, DOI: 10.4049/jimmunol.1800611.Peer-Reviewed Original ResearchConceptsClassical class I moleculesC-terminusNonmammalian vertebratesChicken MHC class IC-terminal endExpressed class I moleculeClass I moleculesPeptide-binding groovePeptides to T lymphocytesJawed vertebratesClass II moleculesArg residuesChicken MHCI moleculesMHC class I allelesRepertoire of peptidesVertebratesPeptide C-terminusII moleculesMammalsClassical class II moleculesClass I allelesPeptideArgI allelesNovel Arginine-containing Macrocyclic MMP Inhibitors: Synthesis, 99mTc-labeling, and Evaluation
Ye Y, Toczek J, Gona K, Kim HY, Han J, Razavian M, Golestani R, Zhang J, Wu TL, Ghosh M, Jung JJ, Sadeghi MM. Novel Arginine-containing Macrocyclic MMP Inhibitors: Synthesis, 99mTc-labeling, and Evaluation. Scientific Reports 2018, 8: 11647. PMID: 30076321, PMCID: PMC6076275, DOI: 10.1038/s41598-018-29941-2.Peer-Reviewed Original ResearchConceptsMatrix metalloproteinasesMMP inhibitorsLung tissueTransgenic miceMMP activityHigh radiochemical purityHydroxamate MMP inhibitorsNumber of diseasesTissue remodelingSimilar inhibition potencyPotent inhibitionTherapySpecific bindingInhibitorsMolecular imagingImagingNovel arginineRadiochemical purityTissueHigh radiochemical yieldNew arginine
2017
Activation of Secretagogue Independent Gastric Acid Secretion via Endothelial Nitric Oxide Synthase Stimulation in Rats
Kitay AM, Link A, Geibel JP. Activation of Secretagogue Independent Gastric Acid Secretion via Endothelial Nitric Oxide Synthase Stimulation in Rats. Cellular Physiology And Biochemistry 2017, 44: 1606-1615. PMID: 29212068, DOI: 10.1159/000485755.Peer-Reviewed Original ResearchConceptsNitric oxide synthaseGastric acid secretionAcid secretionL-arginineL-NAMENO/sGC/cGMP pathwayNitric oxideSGC/cGMP pathwayParietal cellsNitric oxide synthase stimulationSGC inhibitor ODQL-arginine exposureAcid-related diseasesPossible intracellular mechanismsNovel secretagogueRat parietal cellsIsolated gastric glandsUlcer diseaseOxide synthaseCGMP pathwayImmune functionImportant mediatorIntracellular mechanismsSecretionGastric glandsMitochondrial Dysfunction, Through Impaired Autophagy, Leads to Endoplasmic Reticulum Stress, Deregulated Lipid Metabolism, and Pancreatitis in Animal Models
Biczo G, Vegh ET, Shalbueva N, Mareninova OA, Elperin J, Lotshaw E, Gretler S, Lugea A, Malla SR, Dawson D, Ruchala P, Whitelegge J, French SW, Wen L, Husain SZ, Gorelick FS, Hegyi P, Rakonczay Z, Gukovsky I, Gukovskaya AS. Mitochondrial Dysfunction, Through Impaired Autophagy, Leads to Endoplasmic Reticulum Stress, Deregulated Lipid Metabolism, and Pancreatitis in Animal Models. Gastroenterology 2017, 154: 689-703. PMID: 29074451, PMCID: PMC6369139, DOI: 10.1053/j.gastro.2017.10.012.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsArginineAutophagyBile Acids and SaltsCalcium SignalingCeruletideCholine DeficiencyCyclophilinsDisease Models, AnimalEndoplasmic Reticulum StressEthionineGenetic Predisposition to DiseaseHumansLipid MetabolismMembrane Potential, MitochondrialMice, Inbred C57BLMice, KnockoutMitochondriaMitochondrial Proton-Translocating ATPasesPancreasPancreatitisPeptidyl-Prolyl Isomerase FPhenotypeRatsTime FactorsTrehaloseConceptsDevelopment of APAcute pancreatitisEndoplasmic reticulum stressLipid metabolismImpaired autophagyMitochondrial dysfunctionAnimal modelsL-arginine-induced pancreatitisTreatment of APCyclophilin D knockout micePathogenesis of APAdministration of trehalosePancreatic ER stressParameters of pancreatitisReticulum stressSevere acute pancreatitisPancreas of miceDifferent animal modelsER stressPrincipal downstream effectorPancreatic injuryPathologic responsePancreatitis tissuesCyclophilin DNormal pancreasCellular differentiation state modulates the mRNA export activity of SR proteins
Botti V, McNicoll F, Steiner MC, Richter FM, Solovyeva A, Wegener M, Schwich OD, Poser I, Zarnack K, Wittig I, Neugebauer KM, Müller-McNicoll M. Cellular differentiation state modulates the mRNA export activity of SR proteins. Journal Of Cell Biology 2017, 216: 1993-2009. PMID: 28592444, PMCID: PMC5496613, DOI: 10.1083/jcb.201610051.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAnimalsArginineCell DifferentiationCell NucleusDNA-Binding ProteinsHeLa CellsHumansImmunoprecipitationMethylationMiceNeurogenesisPhenotypePhosphorylationPluripotent Stem CellsProtein BindingProtein Processing, Post-TranslationalRepressor ProteinsRNA InterferenceRNA-Binding ProteinsRNA, MessengerSerine-Arginine Splicing FactorsTandem Mass SpectrometryTranscription FactorsTransfectionConceptsMRNA export activitySR proteinsP19 cellsMRNA exportSR protein family membersProtein-RNA interactionsMurine P19 cellsCellular differentiation stateProtein family membersLower phosphorylation levelsArginine methylationPluripotency factorsCytoplasmic mRNA levelsMRNA processingPosttranslational modificationsCellular dynamicsDifferentiated cellsNeural differentiationSRSF5Differentiation statePhosphorylation levelsHeLa cellsProteinExport activityMRNA levelsAcquired Amino Acid Deficiencies: A Focus on Arginine and Glutamine
Morris C, Hamilton‐Reeves J, Martindale R, Sarav M, Gautier J. Acquired Amino Acid Deficiencies: A Focus on Arginine and Glutamine. Nutrition In Clinical Practice 2017, 32: 30s-47s. PMID: 28388380, DOI: 10.1177/0884533617691250.Peer-Reviewed Original ResearchConceptsLow arginine bioavailabilityT cell dysfunctionAmino acidsSickle cell diseaseArginine bioavailabilityPulmonary hypertensionT cellsTherapeutic optionsConditionally essential amino acidsDeficiency syndromeCystic fibrosisEndothelial dysfunctionAcute asthmaAt-risk populationsCatabolic stateCell diseaseClinical scenariosAmino acid synthesisCritical illnessConditions of stressGastrointestinal disordersAcid deficiencyCardiovascular diseaseCatabolism of arginineSynthesized de novoNeonatal nonepileptic myoclonus is a prominent clinical feature of KCNQ2 gain‐of‐function variants R201C and R201H
Mulkey SB, Ben‐Zeev B, Nicolai J, Carroll JL, Grønborg S, Jiang Y, Joshi N, Kelly M, Koolen DA, Mikati MA, Park K, Pearl PL, Scheffer IE, Spillmann RC, Taglialatela M, Vieker S, Weckhuysen S, Cooper EC, Cilio MR. Neonatal nonepileptic myoclonus is a prominent clinical feature of KCNQ2 gain‐of‐function variants R201C and R201H. Epilepsia 2017, 58: 436-445. PMID: 28139826, PMCID: PMC5339037, DOI: 10.1111/epi.13676.Peer-Reviewed Original ResearchConceptsNonepileptic myoclonusClinical presentationFunction variantsMultifocal epileptiform dischargesProminent clinical featureDistinct clinical presentationsProfound developmental delayBurst-suppression patternInstitutional review boardNeonatal encephalopathyClinical featuresEpileptic spasmsNeonatal periodNeonatal seizuresRespiratory dysfunctionPatient RegistryMedical recordsNeonatal presentationElectrophysiologic propertiesEpileptiform dischargesParoxysmal movementsTherapeutic approachesPatientsBrain volumeMyoclonus
2016
Comparison of symmetric dimethylarginine with creatinine, cystatin C and their eGFR equations as markers of kidney function
El-Khoury JM, Bunch DR, Hu B, Payto D, Reineks EZ, Wang S. Comparison of symmetric dimethylarginine with creatinine, cystatin C and their eGFR equations as markers of kidney function. Clinical Biochemistry 2016, 49: 1140-1143. PMID: 27452178, DOI: 10.1016/j.clinbiochem.2016.07.009.Peer-Reviewed Original ResearchConceptsGlomerular filtration rateKidney functionCystatin CEGFR equationsWidespread clinical useIothalamate clearanceEGFR formulasFiltration rateSymmetric dimethylargininePlasma specimensAdult populationStrong markerAbstractTextClinical useEndogenous markerCreatinineLiquid chromatography-tandem mass spectrometry methodChromatography-tandem mass spectrometry methodFurther studiesDimethylarginineRoche Cobas 8000MarkersCatabolic productsCobas 8000
2015
Angiotensin converting enzyme inhibition increases ADMA concentration in patients on maintenance hemodialysis – a randomized cross-over study
Gamboa JL, Pretorius M, Sprinkel KC, Brown NJ, Ikizler TA. Angiotensin converting enzyme inhibition increases ADMA concentration in patients on maintenance hemodialysis – a randomized cross-over study. BMC Nephrology 2015, 16: 167. PMID: 26494370, PMCID: PMC4618919, DOI: 10.1186/s12882-015-0162-x.Peer-Reviewed Original ResearchConceptsEnd-stage renal diseaseAngiotensin receptor blockersMaintenance hemodialysisCross-over studyADMA levelsAsymmetric dimethylarginineACE inhibitionADMA productionADMA concentrationsShort-term ACE inhibitionRandomized cross-over studyIntracellular ADMA concentrationStudy of patientsEffect of bradykininB2 receptor stimulationACE inhibitor-induced increaseInhibitor-induced increaseRamipril treatmentCardiovascular morbidityReceptor blockersEndothelial dysfunctionRenal diseaseBradykinin levelsBackgroundEndothelial dysfunctionDialysis session
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply