2018
Glucose metabolism mediates disease tolerance in cerebral malaria
Wang A, Huen SC, Luan HH, Baker K, Rinder H, Booth CJ, Medzhitov R. Glucose metabolism mediates disease tolerance in cerebral malaria. Proceedings Of The National Academy Of Sciences Of The United States Of America 2018, 115: 11042-11047. PMID: 30291189, PMCID: PMC6205430, DOI: 10.1073/pnas.1806376115.Peer-Reviewed Original ResearchConceptsCerebral malariaGlucose metabolismBlood-brain barrier permeabilityAlternative fuel substrateCerebral malaria modelInflammation-induced anorexiaParasitic disease malariaVehicle-treated animalsAcute inflammatory conditionsTissue-protective mechanismsPotential therapeutic targetDifferent inflammatory statesInhibition of glycolysisViral inflammationANKA infectionThrombotic complicationsInfectious inflammationInflammatory stateBacterial inflammationImmune infiltrationInflammatory conditionsInflammatory diseasesMale miceBarrier permeabilitySickness behavior
2013
Sciatic nerve regeneration is not inhibited by anti-NGF antibody treatment in the adult rat
Lankford K, Arroyo E, Liu C, Somps C, Zorbas M, Shelton D, Evans M, Hurst S, Kocsis J. Sciatic nerve regeneration is not inhibited by anti-NGF antibody treatment in the adult rat. Neuroscience 2013, 241: 157-169. PMID: 23531437, DOI: 10.1016/j.neuroscience.2013.03.024.Peer-Reviewed Original ResearchConceptsNerve growth factorAdult ratsNerve regenerationFunctional recoveryAnti-NGF antibody treatmentElevated nerve growth factorUnilateral sciatic nerve crushDorsal root ganglion neuronsAnti-NGF antibodySciatic nerve crushType of painVehicle-treated animalsSciatic nerve regenerationPost nerve injuryNovel therapeutic approachesCell body sizePeripheral nerve regenerationFluro-GoldPeripheral nervous system developmentNerve injuryPain modelNerve crushPain managementAntibody treatmentGait recovery
2010
Triptolide reduces cyst formation in a neonatal to adult transition Pkd1 model of ADPKD
Leuenroth SJ, Bencivenga N, Chahboune H, Hyder F, Crews CM. Triptolide reduces cyst formation in a neonatal to adult transition Pkd1 model of ADPKD. Nephrology Dialysis Transplantation 2010, 25: 2187-2194. PMID: 20139063, PMCID: PMC2902895, DOI: 10.1093/ndt/gfp777.Peer-Reviewed Original ResearchMeSH KeywordsAgingAnimalsAntineoplastic Agents, AlkylatingCell ProliferationCyclin-Dependent Kinase Inhibitor p21Disease Models, AnimalDisease ProgressionDiterpenesEpoxy CompoundsGTP-Binding ProteinsIntegrasesKidneyMiceMice, Mutant StrainsMutationMyxovirus Resistance ProteinsPhenanthrenesPolycystic Kidney, Autosomal DominantTime FactorsTRPP Cation ChannelsConceptsAutosomal dominant polycystic kidney diseaseCyst formationModel of ADPKDEnd-stage renal failureBlood urea nitrogen levelsPostnatal days P10Vehicle-treated animalsNumber of microcystsUrea nitrogen levelsDominant polycystic kidney diseaseNumerous rodent modelsInducible mouse modelPolycystic kidney diseaseCystic burdenPkd1-deficient miceRenal functionDrug development studiesRenal failureLiver cystsKidney diseaseDaily injectionsCyst progressionDisease progressionNovel therapiesRodent models
2009
Early microglial inhibition preemptively mitigates chronic pain development after experimental spinal cord injury.
Tan AM, Zhao P, Waxman SG, Hains BC. Early microglial inhibition preemptively mitigates chronic pain development after experimental spinal cord injury. The Journal Of Rehabilitation Research And Development 2009, 46: 123. PMID: 19533525, DOI: 10.1682/jrrd.2008.03.0048.Peer-Reviewed Original ResearchConceptsSpinal cord injuryMicroglial activationMinocycline treatmentChronic painCord injuryAdult male Sprague-Dawley ratsLumbar dorsal horn neuronsExperimental spinal cord injuryMale Sprague-Dawley ratsDorsal horn neuronsChronic pain developmentDevelopment of painVehicle-treated animalsSprague-Dawley ratsThoracic spinal segmentsNew therapeutic strategiesQuality of lifeMicroglial inhibitionSCI painMinocycline administrationPain developmentEarly administrationPain conditionsMicroglial signalingDays postinjury
2004
The Effect of Aging on the Skeletal Response to Intermittent Treatment with Parathyroid Hormone
Knopp E, Troiano N, Bouxsein M, Sun BH, Lostritto K, Gundberg C, Dziura J, Insogna K. The Effect of Aging on the Skeletal Response to Intermittent Treatment with Parathyroid Hormone. Endocrinology 2004, 146: 1983-1990. PMID: 15618351, DOI: 10.1210/en.2004-0770.Peer-Reviewed Original ResearchConceptsBody bone mineral densitySkeletal responseAged animalsIntermittent treatmentTotal body bone mineral densityYoung adult C57BL/6 miceDaily sc injectionsVehicle-treated animalsTrabecular bone volume fractionYoung adult miceBone mineral densityYoung adult animalsVertebral histomorphometryEffect of ageBone volume fractionParathyroid hormoneC57BL/6 miceSC injectionPTH treatmentMineral densityBody weightOsteoblast numberPTHCultured marrowYounger counterpartsHistone deacetylase inhibitor suberoylanilide hydroxamic acid reduces acute graft-versus-host disease and preserves graft-versus-leukemia effect
Reddy P, Maeda Y, Hotary K, Liu C, Reznikov L, Dinarello C, Ferrara J. Histone deacetylase inhibitor suberoylanilide hydroxamic acid reduces acute graft-versus-host disease and preserves graft-versus-leukemia effect. Proceedings Of The National Academy Of Sciences Of The United States Of America 2004, 101: 3921-3926. PMID: 15001702, PMCID: PMC374345, DOI: 10.1073/pnas.0400380101.Peer-Reviewed Original ResearchConceptsBone marrow transplantationSuberoylanilide hydroxamic acidAdministration of SAHAProinflammatory cytokinesGVL activityAcute graftHost diseaseHost antigensTime of BMTAllogeneic bone marrow transplantationDonor/recipient combinationsEffects of SAHACytotoxic T cell responsesCytotoxic responseBeneficial GVL effectLeukemia-free survivalT cell proliferativeHistone deacetylase inhibitor suberoylanilide hydroxamic acidT cell responsesVehicle-treated animalsGastrointestinal tract integrityInhibitor suberoylanilide hydroxamic acidHistone deacetylase inhibitionAcute GVHDGVL effect
1995
Effects of brain‐derived neurotrophic factor on motor dysfunction in wobbler mouse motor neuron disease
Ikeda K, Klinkosz B, Greene T, Cedarbaum J, Wong V, Lindsay R, Mitsumoto H. Effects of brain‐derived neurotrophic factor on motor dysfunction in wobbler mouse motor neuron disease. Annals Of Neurology 1995, 37: 505-511. PMID: 7717687, DOI: 10.1002/ana.410370413.Peer-Reviewed Original ResearchConceptsBrain-derived neurotrophic factorMouse motor neuron diseaseWobbler mouse motor neuron diseaseMotor neuron diseaseBDNF treatmentMotor dysfunctionNeurotrophic factorNeuron diseaseVentral rootsMotor neuronsWobbler miceExogenous brain-derived neurotrophic factorAxotomy-induced cell deathHuman brain-derived neurotrophic factorBDNF-treated miceBiceps muscle weightCervical ventral rootsDenervation muscle atrophyExogenous BDNF administrationMotor axon lossRecombinant human brain-derived neurotrophic factorVehicle-treated miceVehicle-treated animalsEnd of treatmentMuscle twitch tension
1994
The effects of ciliary neurotrophic factor on motor dysfunction in wobbler mouse motor neuron disease
Mitsumoto H, Ikeda K, Holmlund T, Greene T, Cedarbaum J, Wong V, Lindsay R. The effects of ciliary neurotrophic factor on motor dysfunction in wobbler mouse motor neuron disease. Annals Of Neurology 1994, 36: 142-148. PMID: 8053649, DOI: 10.1002/ana.410360205.Peer-Reviewed Original ResearchConceptsCiliary neurotrophic factorNeurotrophic factorMotor neuron diseaseHuman ciliary neurotrophic factorGrip strengthNeuron diseaseBody weightWobbler mouse motor neuron diseaseMotor neuron disease modelMouse motor neuron diseaseFirst neurotrophic factorMean grip strengthImproved muscle strengthVehicle-treated animalsWeeks of treatmentMuscle twitch tensionSurvival-promoting effectsWobbler mouse modelRat ciliary neurotrophic factorMotor dysfunctionControl miceMuscle strengthDisease progressionMotor neuronsTwitch tension
1993
Depolarization inactivation of dopamine neurons: Terminal release characteristics
Moghaddam B, Bunney B. Depolarization inactivation of dopamine neurons: Terminal release characteristics. Synapse 1993, 14: 195-200. PMID: 8105547, DOI: 10.1002/syn.890140302.Peer-Reviewed Original ResearchConceptsExtracellular dopamine levelsChronic haloperidol treatmentDopamine levelsHaloperidol treatmentExtracellular levelsPerfusion of tetrodotoxinExcitatory amino acidsStriatal extracellular levelsVehicle-treated animalsExtracellular glutamate levelsHaloperidol-treated animalsMedial forebrain bundleStriatal dopamine systemGroups of animalsExogenous antagonistsChronic haloperidolChronic treatmentDepolarization inactivationExcitatory actionBasal outflowDopamine neuronsGlutamate levelsImpulse flowForebrain bundleMicrodialysis technique
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