2025
Prenatal opioid exposure alters pain perception and increases long-term health risks in infants with neonatal opioid withdrawal syndrome
Radhakrishna U, Radhakrishnan R, Uppala L, Trivedi T, Prajapati J, Rawal R, Muvvala S, Bahado-Singh R, Sadhasivam S. Prenatal opioid exposure alters pain perception and increases long-term health risks in infants with neonatal opioid withdrawal syndrome. Frontiers In Pain Research 2025, 6: 1497801. PMID: 40313396, PMCID: PMC12043715, DOI: 10.3389/fpain.2025.1497801.Peer-Reviewed Original ResearchNeonatal opioid withdrawal syndromeOpioid-exposed infantsOpioid withdrawal syndromePain-related genesOpioid exposureWithdrawal syndromeChronic painEpigenetic changesMaternal opioid exposurePrenatal opioid exposureImprove pain managementIon channel functionIllumina Infinium Methylation EPIC BeadChipInfinium Methylation EPIC BeadChipAnalyzed DNA methylationUnexposed control subjectsLong-term health risksPain reliefPain perceptionPregnant womenGnRH secretionPlacental tissueMorphine addictionHealth of mothersControl subjectsVentricular ion channels and arrhythmias: an overview of physiology, pathophysiology and pharmacology
Liu S, Wang W, Yang Y, Huang Z. Ventricular ion channels and arrhythmias: an overview of physiology, pathophysiology and pharmacology. Medical Review 2025, 5: 231-243. PMID: 40600182, PMCID: PMC12207207, DOI: 10.1515/mr-2024-0085.Peer-Reviewed Original ResearchCardiac ion channelsAntiarrhythmic drugsIon channelsAssociated with inherited cardiac arrhythmiasAction potentialsVentricular ion channelsCardiac action potentialIon channel functionCardiac functionNa VChannel functionOverview of physiologyCardiac arrhythmiasDysfunctional mutationsGenetic mutationsArrhythmiasTherapeutic targetPropagation of cardiac action potentialsCardiac electrophysiologyCa VPathophysiologyCardiac healthDrugPharmacologyMutations
2021
An ammonium transporter is a non-canonical olfactory receptor for ammonia
Vulpe A, Kim HS, Ballou S, Wu ST, Grabe V, Nava Gonzales C, Liang T, Sachse S, Jeanne JM, Su CY, Menuz K. An ammonium transporter is a non-canonical olfactory receptor for ammonia. Current Biology 2021, 31: 3382-3390.e7. PMID: 34111404, PMCID: PMC8355169, DOI: 10.1016/j.cub.2021.05.025.Peer-Reviewed Original ResearchConceptsOlfactory receptorsGenetic model organism Drosophila melanogasterModel organism Drosophila melanogasterAmmonium transporter familyCanonical olfactory receptorsIon channel functionAmmonium transportersInsect speciesDrosophila melanogasterMost insectsMutant fliesFirst transporterParticular olfactory receptorTransporter familyAgricultural pestsHematophagous insectsEctopic expressionDrosophilaInsectsChannel functionWidespread importanceAmmonia sensitivitySpeciesTransportersReceptors
2018
C-terminal proline deletions in KCNC3 cause delayed channel inactivation and an adult-onset progressive SCA13 with spasticity
Khare S, Galeano K, Zhang Y, Nick JA, Nick HS, Subramony SH, Sampson J, Kaczmarek LK, Waters MF. C-terminal proline deletions in KCNC3 cause delayed channel inactivation and an adult-onset progressive SCA13 with spasticity. The Cerebellum 2018, 17: 692-697. PMID: 29949095, PMCID: PMC8299775, DOI: 10.1007/s12311-018-0950-5.Peer-Reviewed Original ResearchConceptsIon channel functionMammalian cell cultureMutant proteinsIntracellular cSpinocerebellar ataxia 13Autosomal dominant neurological diseaseChannel functionAllelic heterogeneityProline deletionSCA13 patientsTerminal portionProgressive clinical symptomsNormal membranesCell culturesProteinElectrophysiological characterizationChannel inactivationInactivationClinical symptomsElectrophysiological profileNeurological diseasesClinical importanceSCA13Slow inactivationDeletion
2013
Mitochondrial targets for arrhythmia suppression: is there a role for pharmacological intervention?
Akar FG. Mitochondrial targets for arrhythmia suppression: is there a role for pharmacological intervention? Journal Of Interventional Cardiac Electrophysiology 2013, 37: 249-258. PMID: 23824789, DOI: 10.1007/s10840-013-9809-3.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsMitochondrial targetsMitochondrial dysfunctionCritical cellular functionsCell death pathwaysCellular redox statusIon channel functionMitochondrial networkCellular functionsDeath pathwaysMitochondrial originIschemia-reperfusion injuryCommon cardiovascular disordersMitochondrial bioenergeticsExcitation-contraction couplingChannel functionRedox statusMechanistic linkHeart failureArrhythmia suppressionPharmacological interventionsCardiovascular disordersCentral mechanismsDysfunctionArrhythmogenesisEnergy production
2005
Ion channels as novel therapeutic targets in heart failure
Akar FG, Tomaselli GF. Ion channels as novel therapeutic targets in heart failure. Annals Of Medicine 2005, 37: 44-54. PMID: 15902846, DOI: 10.1080/07853890510007214.Peer-Reviewed Original ResearchConceptsHeart failureIon channel functionAnti-arrhythmic therapyLethal ventricular tachyarrhythmiasCalcium handling proteinsNovel therapeutic targetPublic health epidemicIon channel dysfunctionChannel functionVentricular tachyarrhythmiasTherapeutic targetChannel dysfunctionHandling proteinsSodium currentHealth epidemicNovel targetImpulse generationElectrical phenotypeIon channelsCurrent understandingTachyarrhythmiasFailureDysfunctionTherapyAbnormalities
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