2008
Activation of brain protein phosphatase‐1I following cardiac arrest and resuscitation involving an interaction with 14‐3‐3γ
Platholi J, Heerdt PM, Tung H, Hemmings HC. Activation of brain protein phosphatase‐1I following cardiac arrest and resuscitation involving an interaction with 14‐3‐3γ. Journal Of Neurochemistry 2008, 105: 2029-2038. PMID: 18284617, PMCID: PMC3872065, DOI: 10.1111/j.1471-4159.2008.05300.x.Peer-Reviewed Original ResearchConceptsGlobal cerebral ischemiaCerebral ischemiaCardiac arrestTransient global cerebral ischemiaTransient cerebral ischemiaPotential therapeutic targetRelevant pig modelIschemic brainNeuroprotective mechanismsControl brainsInhibitory modulatorTherapeutic targetPig modelIschemiaPig brainBrain proteinsMechanism-based approachBrainProtein betaResuscitationEnergy metabolismCritical regulatorArrestVivoActivationProtein phosphatase-2A is activated in pig brain following cardiac arrest and resuscitation
Zhang TT, Platholi J, Heerdt PM, Hemmings HC, Tung HY. Protein phosphatase-2A is activated in pig brain following cardiac arrest and resuscitation. Metabolic Brain Disease 2008, 23: 95-104. PMID: 18197471, DOI: 10.1007/s11011-007-9074-1.Peer-Reviewed Original Research
2007
Protein phosphatase‐1I activation in brain following cardiac arrest and resuscitation
Platholi J, Heerdt P, Tung H, Hemmings H. Protein phosphatase‐1I activation in brain following cardiac arrest and resuscitation. The FASEB Journal 2007, 21: a618-a619. DOI: 10.1096/fasebj.21.5.a618-d.Peer-Reviewed Original ResearchProtein phosphatase 1Cerebral ischemiaCellular energy metabolismPig brainApoptotic cell deathTransient global cerebral ischemiaPhosphatase 1Protein regulatorsGlobal cerebral ischemiaPP-1Major proteinsInhibitor 2Cell deathSubunit compositionEnergy metabolismIntact animal modelIonic balanceCardiac arrestAnimal modelsProtective mechanismBrainIschemiaDeathDependent formRegulator
2000
Isoflurane Pretreatment Ameliorates Postischemic Neurologic Dysfunction and Preserves Hippocampal Ca2+/Calmodulin-dependent Protein Kinase in a Canine Cardiac Arrest Model
Blanck T, Haile M, Xu F, Zhang J, Heerdt P, Veselis R, Beckman J, Kang R, Adamo A, Hemmings H. Isoflurane Pretreatment Ameliorates Postischemic Neurologic Dysfunction and Preserves Hippocampal Ca2+/Calmodulin-dependent Protein Kinase in a Canine Cardiac Arrest Model. Anesthesiology 2000, 93: 1285-1293. PMID: 11046218, DOI: 10.1097/00000542-200011000-00023.Peer-Reviewed Original ResearchMeSH KeywordsAnesthetics, InhalationAnimalsBlood PressureBlotting, WesternBrain DiseasesCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium-Calmodulin-Dependent Protein KinasesDogsFemaleHeart Arrest, InducedHeart RateHippocampusIschemic Attack, TransientIschemic PreconditioningIsofluraneNeuroprotective AgentsSynaptosomesConceptsNeurologic deficit scoreCanine cardiac arrest modelCardiac arrest modelDeficit scoresIschemic animalsCardiac arrestGlobal ischemiaStriatum of animalsEffective neuroprotective drugsIsoflurane pretreatmentNeurologic dysfunctionNeurologic functionHippocampal contentNeuroprotective effectsIsoflurane exposureHippocampal levelsIntensive careNeuroprotective drugsRat modelVentricular fibrillationInhalational anestheticsTreatment groupsBlinded evaluatorsCanine modelIschemia