2016
Enhanced hypoxic tolerance by Seabuckthorn is due to upregulation of HIF-1α and attenuation of ER stress
Jain K, Suryakumar G, Prasad R, Ganju L, Singh S. Enhanced hypoxic tolerance by Seabuckthorn is due to upregulation of HIF-1α and attenuation of ER stress. Journal Of Applied Biomedicine 2016, 14: 71-83. DOI: 10.1016/j.jab.2015.10.001.Peer-Reviewed Original ResearchHIF-1αHypoxic toleranceER stressAnti-inflammatory effectsPro-survival effectsFree radical productionCardioprotective actionCardiac damageHO-1NF-κBHerbal supplementsKey adaptive responseOxidative stressTwo-fold increaseHsp70 levelsAntioxidant potentialProtein carbonylationRadical productionHypoxiaSignificant declineSignaling cascadesAdaptive responseCross talkNovel insightsRedox homeostasis
2008
Fuel utilization by hypothalamic neurons: roles for ROS
Horvath TL, Andrews ZB, Diano S. Fuel utilization by hypothalamic neurons: roles for ROS. Trends In Endocrinology And Metabolism 2008, 20: 78-87. PMID: 19084428, DOI: 10.1016/j.tem.2008.10.003.Peer-Reviewed Original ResearchConceptsEnergy homeostasisFree radical productionAnorexigenic neuronsNeuronal doctrineArcuate nucleusHypothalamic neuronsHypothalamic outputMelanocortin systemEffect of glucoseNeuronal functionFree radical formationSpecific neuronsAcid levelsNeuronsAmino acid levelsNeurobiological aspectsRadical productionEvidence pointsFatty acidsFuel sensingIntracellular substratesHomeostasisNutritional signalsGlucoseHypothalamus
2005
Mitochondrial uncoupling proteins in the cns: in support of function and survival
Andrews ZB, Diano S, Horvath TL. Mitochondrial uncoupling proteins in the cns: in support of function and survival. Nature Reviews Neuroscience 2005, 6: 829-840. PMID: 16224498, DOI: 10.1038/nrn1767.Peer-Reviewed Original ResearchConceptsNeuronal functionNeurological disordersTraumatic brain injuryAmyotrophic lateral sclerosisClinical treatment strategiesMitochondrial calcium influxModels of neurodegenerationMitochondrial uncouplingFree radical productionReactive oxygen species productionNeuronal deteriorationNeuronal deathSubstantia nigraBrain injurySpinal cordVentral tegmentumTreatment strategiesOxygen species productionNeuronal microenvironmentSynaptic transmissionCalcium influxLimbic systemNeurological conditionsLateral sclerosisParkinson's diseaseOral allopurinol does not prevent the frequency or the severity of post-ERCP pancreatitis
Mosler P, Sherman S, Marks J, Watkins JL, Geenen JE, Jamidar P, Fogel EL, Lazzell-Pannell L, Temkit M, Tarnasky P, Block KP, Frakes JT, Aziz AA, Malik P, Nickl N, Slivka A, Goff J, Lehman GA. Oral allopurinol does not prevent the frequency or the severity of post-ERCP pancreatitis. Gastrointestinal Endoscopy 2005, 62: 245-250. PMID: 16046988, DOI: 10.1016/s0016-5107(05)01572-5.Peer-Reviewed Original ResearchConceptsPost-ERCP pancreatitisOral allopurinolAllopurinol groupControl groupOxygen-derived free radical productionPlacebo 4 hoursProcedure risk factorsCommon major complicationSeverity of pancreatitisFree radical productionProphylactic allopurinolPatient demographicsMajor complicationsOverall incidencePostprocedure pancreatitisPharmacologic agentsRisk factorsPancreatitisPatientsStandardized criteriaAllopurinolERCPSeveritySignificant differencesIncidence
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