2024
A kidney-hypothalamus axis promotes compensatory glucose production in response to glycosuria
Faniyan T, Zhang X, Morgan D, Robles J, Bathina S, Brookes P, Rahmouni K, Perry R, Chhabra K. A kidney-hypothalamus axis promotes compensatory glucose production in response to glycosuria. ELife 2024, 12 DOI: 10.7554/elife.91540.4.Peer-Reviewed Original ResearchGlucose productionEndogenous glucose productionReabsorption of nutrientsLoss of glucoseHypothalamic-pituitary-adrenal axisNormal energy supplyProteomic analysisCompensatory increaseAfferent renal nervesAfferent renal denervationPlasma proteomic analysisDefense mechanismsAcute phase proteinsRenal denervationKO miceSGLT2 inhibitorsKnockout miceRenal nervesAfferent nervesEfficiency of drugsBody's defense mechanismsGlycosuriaGlucosePhase proteinsTreat hyperglycemia
2020
Atrial Function and Its Role in the Non-invasive Evaluation of Diastolic Function in Congenital Heart Disease
Ta HT, Alsaied T, Steele JM, Truong VT, Mazur W, Nagueh SF, Kutty S, Tretter JT. Atrial Function and Its Role in the Non-invasive Evaluation of Diastolic Function in Congenital Heart Disease. Pediatric Cardiology 2020, 41: 654-668. PMID: 32342149, DOI: 10.1007/s00246-020-02351-w.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsCongenital heart diseaseAtrial functionDiastolic functionNon-invasive assessmentHeart diseaseDiastolic dysfunctionVentricular diastolic dysfunctionDiastolic function assessmentNon-invasive evaluationAtrial dysfunctionAdult patientsAtrial sizeAdverse outcomesConduit functionBody of evidenceContractile functionFunction assessmentCompensatory increaseDysfunctionCommon pathwayDiseaseAtrial formCurrent knowledgePivotal roleMost forms
2019
Glutamate Signaling in Hepatic Stellate Cells Drives Alcoholic Steatosis
Choi W, Kim H, Kim M, Cinar R, Yi H, Eun H, Kim S, Choi Y, Lee Y, Kim S, Seo W, Lee J, Shim Y, Kim Y, Yang K, Ryu T, Hwang J, Lee C, Choi H, Gao B, Kim W, Kim S, Kunos G, Jeong W. Glutamate Signaling in Hepatic Stellate Cells Drives Alcoholic Steatosis. Cell Metabolism 2019, 30: 877-889.e7. PMID: 31474565, PMCID: PMC6834910, DOI: 10.1016/j.cmet.2019.08.001.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAmino Acid Transport System y+AnimalsArachidonic AcidsEndocannabinoidsFatty Liver, AlcoholicFemaleGlutamic AcidGlyceridesHEK293 CellsHep G2 CellsHepatic Stellate CellsHepatocytesHumansLipogenesisMaleMiceMice, Inbred C57BLMice, KnockoutMiddle AgedReceptor, Cannabinoid, CB1Receptor, Metabotropic Glutamate 5Signal TransductionTransfectionConceptsAlcoholic liver diseaseExpression of metabotropic glutamate receptor 5Pharmacological inhibition of mGluR5Metabotropic glutamate receptor 5Alcoholic steatosisCannabinoid receptor 1Glutamate receptor 5Inhibition of mGluR5Extracellular glutamate levelsGlutamate signalingGlutamate levelsHepatic stellate cellsMGluR5Receptor 5Receptor 1Liver diseaseMetabolic synapsePharmacological inhibitionStellate cellsCystine uptakeCompensatory increaseCysteine deficiencyGlutathione depletionSteatosisMiceComputational modeling predicts immuno-mechanical mechanisms of maladaptive aortic remodeling in hypertension
Latorre M, Bersi MR, Humphrey JD. Computational modeling predicts immuno-mechanical mechanisms of maladaptive aortic remodeling in hypertension. International Journal Of Engineering Science 2019, 141: 35-46. PMID: 32831391, PMCID: PMC7437922, DOI: 10.1016/j.ijengsci.2019.05.014.Peer-Reviewed Original ResearchAortic remodelingBlood pressure elevationCentral artery stiffnessMajor risk factorCommon mouse modelsBasic science studiesUncontrolled hypertensionIndicators of diseaseAortic stiffeningPressure elevationAdventitial fibrosisArtery stiffnessAortic growthRisk factorsAbdominal aortaCardiovascular diseaseMouse modelTherapeutic strategiesHypertensionAortic wallCompensatory increaseInflammationFibrosisDiseaseMarked increasePI3K oncogenic mutations mediate resistance to afatinib in HER2/neu overexpressing gynecological cancers
Bonazzoli E, Cocco E, Lopez S, Bellone S, Zammataro L, Bianchi A, Manzano A, Yadav G, Manara P, Perrone E, Haines K, Espinal M, Dugan K, Menderes G, Altwerger G, Han C, Zeybek B, Litkouhi B, Ratner E, Silasi DA, Huang GS, Azodi M, Schwartz PE, Santin AD. PI3K oncogenic mutations mediate resistance to afatinib in HER2/neu overexpressing gynecological cancers. Gynecologic Oncology 2019, 153: 158-164. PMID: 30630630, PMCID: PMC6430698, DOI: 10.1016/j.ygyno.2019.01.002.Peer-Reviewed Original ResearchMeSH KeywordsAdultAfatinibAgedAnimalsAntineoplastic AgentsCell Line, TumorClass I Phosphatidylinositol 3-KinasesClass Ia Phosphatidylinositol 3-KinaseDrug Resistance, NeoplasmFemaleGenital Neoplasms, FemaleHumansMiceMice, SCIDMiddle AgedMutationPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsReceptor, ErbB-2TransfectionXenograft Model Antitumor AssaysConceptsHER2/neuAKT/mTOR pathwayPIK3CA mutationsMTOR pathwayActivity of afatinibEffect of afatinibPI3K/AKT/mTOR pathwayPotential mechanismsPIK3CA/AKT/mTOR pathwayRapid tumor growthGreater compensatory increasePI3K mutationsAmplification/mutationOncogenic PIK3CA mutationsAfatinib exposurePIK3CA H1047RGynecological cancerClinical trialsMTOR inhibitorsAfatinibTumor growthCompensatory increasePhosphorylated Akt proteinPIK3CA geneC-erb
2017
Removing Cerebrospinal Fluid Antibody Orders from the Test Menu Results in a Dramatic Decrease in Order Volume
Beal S, Tremblay E, Harris N, Rand K. Removing Cerebrospinal Fluid Antibody Orders from the Test Menu Results in a Dramatic Decrease in Order Volume. The Journal Of Applied Laboratory Medicine 2017, 2: 47-54. PMID: 33636964, DOI: 10.1373/jalm.2017.023515.Peer-Reviewed Original ResearchCerebrospinal fluidTest menuTest order volumeB. burgdorferiComputerized physician order entry systemPhysician order entry systemTest ordersCMV PCROrder entry systemAntibody testingT. gondiiToxoplasma gondiiParadoxical increaseCompensatory increaseUseful testSubstantial cost savingsBorrelia burgdorferiBurgdorferiGondiiCPOELaboratory testsEntry systemDramatic decreaseProvidersCost savings
2013
Renalase regulates renal dopamine and phosphate metabolism
Sizova D, Velazquez H, Sampaio-Maia B, Quelhas-Santos J, Pestana M, Desir GV. Renalase regulates renal dopamine and phosphate metabolism. American Journal Of Physiology. Renal Physiology 2013, 305: f839-f844. PMID: 23863468, PMCID: PMC3761288, DOI: 10.1152/ajprenal.00616.2012.Peer-Reviewed Original ResearchConceptsRenal DA synthesisKO micePO4 excretionDA synthesisSodium-phosphate cotransporter Npt2aCatecholamine-degrading enzymeIntrinsic renal defectRenal dopamine synthesisWild-type miceKO mice showKnockout mouse modelDopa excretionRenalase deficiencySevere hypophosphatemiaRenal dopamineSerum PO4Urinary dopaminePhosphate excretionRegular dietDietary phosphateDopamine synthesisMouse modelMice showCompensatory increaseRenal defects
2011
Genetic evidence of the regulatory role of parathyroid hormone–related protein in articular chondrocyte maintenance in an experimental mouse model
Macica C, Liang G, Nasiri A, Broadus AE. Genetic evidence of the regulatory role of parathyroid hormone–related protein in articular chondrocyte maintenance in an experimental mouse model. Arthritis & Rheumatism 2011, 63: 3333-3343. PMID: 21702022, PMCID: PMC3197958, DOI: 10.1002/art.30515.Peer-Reviewed Original ResearchConceptsHormone-related proteinDegenerative changesKO miceParathyroid hormone-related proteinMale KO miceExperimental mouse modelMouse articular cartilageTotal histologic scoreIndian hedgehogTibial articular surfaceArticular chondrocytesArticular cartilageGrowth differentiation factor 5Degenerative findingsControl miceHistologic scoresMouse modelCompensatory increaseTime-course studyDifferentiation factor 5PTHrPRegulatory roleMiceConditional deletionChondrocyte maintenance
2010
The Slack Sodium-Activated Potassium Channel Provides a Major Outward Current in Olfactory Neurons of Kv1.3−/− Super-Smeller Mice
Lu S, Das P, Fadool DA, Kaczmarek LK. The Slack Sodium-Activated Potassium Channel Provides a Major Outward Current in Olfactory Neurons of Kv1.3−/− Super-Smeller Mice. Journal Of Neurophysiology 2010, 103: 3311-3319. PMID: 20393063, PMCID: PMC2888249, DOI: 10.1152/jn.00607.2009.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornBiophysicsCardiovascular AgentsCells, CulturedElectric StimulationGene Expression RegulationIn Vitro TechniquesKv1.3 Potassium ChannelMembrane PotentialsMiceMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsNeuronsOlfactory BulbPatch-Clamp TechniquesPotassium ChannelsPotassium Channels, Sodium-ActivatedPyrimidinesRNA InterferenceSodium Channel BlockersTetrodotoxinTransfectionConceptsMitral cellsOlfactory bulbOutward currentsOlfactory neuronsWildtype animalsPotassium channelsMajor outward currentVoltage-clamp recordingsVoltage-dependent potassium channelsNet outward currentIntracellular sodiumOB slicesPotassium channel genesCompensatory increaseFiring patternsWestern blottingRNA interference approachPrimary culturesEnhanced expressionDetection of odorsSame treatmentChannel genesMiceNeuronsOlfactory phenotypes
2007
Bisphenol A Prevents the Synaptogenic Response to Testosterone in the Brain of Adult Male Rats
Leranth C, Szigeti-Buck K, MacLusky NJ, Hajszan T. Bisphenol A Prevents the Synaptogenic Response to Testosterone in the Brain of Adult Male Rats. Endocrinology 2007, 149: 988-994. PMID: 18048497, PMCID: PMC2275360, DOI: 10.1210/en.2007-1053.Peer-Reviewed Original ResearchConceptsAdult male ratsMedial prefrontal cortexMale ratsSpine synapsesCA1 hippocampal areaAsymmetric spine synapsesSham-operated animalsElectron microscopic stereologyImpairs synaptogenesisSynaptogenic actionsOvariectomized ratsHippocampal areaTestosterone supplementationTestosterone propionateEstrogen receptorExposure measurement dataOil vehicleCompensatory increaseIntact animalsSynthetic xenoestrogenPrefrontal cortexRatsHippocampusCastrated malesPotential mechanismsRenalase is a novel renal hormone that regulates cardiovascular function
Desir GV. Renalase is a novel renal hormone that regulates cardiovascular function. International Journal Of Cardiology Cardiovascular Risk And Prevention 2007, 1: 99-103. PMID: 20409839, DOI: 10.1016/j.jash.2006.12.001.Peer-Reviewed Original ResearchChronic kidney diseaseRenal hormoneBlood pressureKidney diseaseBlood levelsFlavin adenine dinucleotide-dependent amine oxidaseEnd-stage renal diseaseRenal replacement therapySystemic blood pressurePeripheral vascular toneCardiovascular morbidityCardiovascular outcomesSympathetic toneRenal diseaseCatecholamine levelsReplacement therapyVascular tonePatient populationCardiac functionDiseased kidneysCardiovascular functionCardiac contractilityHealthy subjectsHeart rateCompensatory increase
2005
Alterations in growth and apoptosis of insulin receptor substrate-1-deficient β-cells
Hennige A, Ozcan U, Okada T, Jhala U, Schubert M, White M, Kulkarni R. Alterations in growth and apoptosis of insulin receptor substrate-1-deficient β-cells. AJP Endocrinology And Metabolism 2005, 289: e337-e346. PMID: 15827066, DOI: 10.1152/ajpendo.00032.2004.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAnimalsApoptosisCell ProliferationInsulinInsulin Receptor Substrate ProteinsInsulin ResistanceIntracellular Signaling Peptides and ProteinsIslets of LangerhansIslets of Langerhans TransplantationKidneyMaleMiceMice, Inbred C57BLMice, KnockoutPhosphoproteinsSignal TransductionConceptsInsulin resistanceInsulin receptor substrateWT recipientsInsulin/IGFIRS-1 knockout miceBeta-cell proliferationBeta-cell apoptosisIslet hypoplasiaIRS-2 expressionEndogenous isletsOvert diabetesKidney capsuleIslet responseIslet functionIslet defectKnockout miceMitotic rateCompensatory increaseIslet growthDysfunctional isletsGrowth retardationTransplantation approachesΒ-cellsAntiapoptotic effectIGFRenalase is a novel, soluble monoamine oxidase that regulates cardiac function and blood pressure
Xu J, Li G, Wang P, Velazquez H, Yao X, Li Y, Wu Y, Peixoto A, Crowley S, Desir GV. Renalase is a novel, soluble monoamine oxidase that regulates cardiac function and blood pressure. Journal Of Clinical Investigation 2005, 115: 1275-1280. PMID: 15841207, PMCID: PMC1074681, DOI: 10.1172/jci24066.Peer-Reviewed Original ResearchConceptsEnd-stage renal diseaseBlood pressureRenal diseaseCardiac functionNovel flavin adenine dinucleotide-dependent amine oxidaseFlavin adenine dinucleotide-dependent amine oxidaseSystemic blood pressurePeripheral vascular toneRenalase gene expressionCardiovascular morbiditySoluble monoamine oxidaseVascular toneAvailable therapiesPlasma concentrationsCardiac contractilityEndocrine functionEndocrine organHealthy subjectsHeart rateElectrolyte balanceCompensatory increaseSmall intestineKidneyRenalaseMonoamine oxidase
2002
Defective insulin secretion in pancreatic β cells lacking type 1 IGF receptor
Xuan S, Kitamura T, Nakae J, Politi K, Kido Y, Fisher P, Morroni M, Cinti S, White M, Herrera P, Accili D, Efstratiadis A. Defective insulin secretion in pancreatic β cells lacking type 1 IGF receptor. Journal Of Clinical Investigation 2002, 110: 1011-1019. PMID: 12370279, PMCID: PMC151144, DOI: 10.1172/jci15276.Peer-Reviewed Original ResearchConceptsType 1 IGF receptorBeta-cell massDefective insulin secretionInsulin secretionIGF receptorInsulin releaseInadequate compensatory increaseGlucose-dependent insulin releaseBeta-cell proliferationAge-dependent impairmentPancreatic β-cellsGlucose toleranceDecrease of glucoseBeta cellsType 2Compensatory increaseCell massΒ-cellsReceptor tyrosine kinasesSecretionCell proliferationAntiapoptotic roleReceptorsTyrosine kinaseConditional mutagenesis
1999
Changes in Bone Turnover in Young Women Consuming Different Levels of Dietary Protein1
Kerstetter J, Mitnick M, Gundberg C, Caseria D, Ellison A, Carpenter T, Insogna K. Changes in Bone Turnover in Young Women Consuming Different Levels of Dietary Protein1. The Journal Of Clinical Endocrinology & Metabolism 1999, 84: 1052-1055. PMID: 10084594, DOI: 10.1210/jcem.84.3.5552.Peer-Reviewed Original ResearchUrinary N-telopeptide excretionBone-specific alkaline phosphataseN-telopeptide excretionUrinary calcium excretionBone turnoverLow-protein dietCalcium excretionUrinary calciumProtein dietBone resorptionDietary proteinYoung womenHealthy young womenNegative calcium balanceLow protein intakeHigh-protein dietAlkaline phosphataseSecondary hyperparathyroidismSerum PTHSerum osteocalcinDihydroxyvitamin DCalcium balanceProtein intakeCompensatory increaseDay 4
1988
Humoral Hypercalcemia of Malignancy in Canine Lymphosarcoma*
Weir EC, Norrdin RW, Matus RE, Brooks MB, Broadus AE, Mitnick M, Johnston SD, Insogna KL. Humoral Hypercalcemia of Malignancy in Canine Lymphosarcoma*. Endocrinology 1988, 122: 602-608. PMID: 2828006, DOI: 10.1210/endo-122-2-602.Peer-Reviewed Original ResearchConceptsAdenylate cyclase-stimulating activityHypercalcemic dogsCanine lymphosarcomaFractional phosphorus excretionEvidence of tumorQuantitative bone histomorphometryBone-resorbing factorsImmunoreactive PTH levelsPathogenesis of hypercalcemiaIliac crest biopsiesTumor tissue extractsCyclase-stimulating activityBone histomorphometric findingsCalcium excretionPTH levelsHumoral hypercalcemiaDihydroxyvitamin DBone resorptionHistomorphometric findingsBone histomorphometryPTH receptorBiopsy siteCrest biopsiesTumor extractsCompensatory increase
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