2025
Scalp rhythmic epileptiform discharges in focal cortical dysplasia: A clinicopathological study
Xu S, Ming W, Hong B, Zhou J, Jin B, Lv J, Zheng Z, Jiang H, Shen C, Wang Z, Wang Y, Ding M, Xu J, Wang S, Zheng Y. Scalp rhythmic epileptiform discharges in focal cortical dysplasia: A clinicopathological study. Clinical Neurophysiology 2025, 174: 10-16. PMID: 40179633, DOI: 10.1016/j.clinph.2025.03.031.Peer-Reviewed Original ResearchConceptsRhythmic epileptiform dischargesFocal cortical dysplasia type 2Focal cortical dysplasiaFavorable surgical outcomeSurgical outcomesCortical dysplasiaEpileptiform dischargesAssociated with favorable surgical outcomesType 2Focal cortical dysplasia patientsChloride transportScalp electroencephalogramResection surgeryInterictal patternsClinical significanceClinical variablesPathologic correlationClinicopathological studyExtratemporal regionsPatientsAbnormal expressionPathological cellsPathological substrateDysplasiaElectroencephalogramCACNA1G, A Heterotaxy Candidate Gene, Plays a Role in Ciliogenesis and Left‐Right Patterning in Xenopus tropicalis
Kostiuk V, Kabir R, Akbari R, Rushing A, González D, Kim A, Kim A, Zenisek D, Khokha M. CACNA1G, A Heterotaxy Candidate Gene, Plays a Role in Ciliogenesis and Left‐Right Patterning in Xenopus tropicalis. Genesis 2025, 63: e70009. PMID: 40008628, PMCID: PMC11867209, DOI: 10.1002/dvg.70009.Peer-Reviewed Original ResearchConceptsCongenital heart diseaseCACNA1GLow-voltage-activated calcium channelsExpression of Cacna1gCalcium channelsPatient cohortCardiac functionLR patterningHeterotaxyLR organizerChannel familyCACNA1SHeart diseaseLeft-rightG expressionXenopus tropicalisAbnormal expressionProcess of cilia formationCardiac loopingMultiple organsSignaling cascadesLR asymmetryPatientsT-typeEmbryonic development
2020
Ectopic HCN4 expression drives mTOR-dependent epilepsy in mice
Hsieh LS, Wen JH, Nguyen LH, Zhang L, Getz SA, Torres-Reveron J, Wang Y, Spencer DD, Bordey A. Ectopic HCN4 expression drives mTOR-dependent epilepsy in mice. Science Translational Medicine 2020, 12 PMID: 33208499, PMCID: PMC9888000, DOI: 10.1126/scitranslmed.abc1492.Peer-Reviewed Original ResearchConceptsFocal cortical dysplasia type IITuberous sclerosis complexFocal cortical malformationsPyramidal neuronsMouse modelHCN4 expressionCortical pyramidal neuronsOnset of seizuresIntracellular cAMP concentrationSeizure activityCortical malformationsRepetitive firingDiseased neuronsSeizuresAbnormal expressionNeuronsEpilepsyCausative linkSeizure mechanismsCAMP concentrationMechanistic targetHCN4Channel activityPatientsGene therapy
2019
Protective effects of GPR120 agonist-programmed macrophages on renal interstitial fibrosis in unilateral ureteral obstruction (UUO) rats
Wang L, Ren X, Tian XF, Cheng XL, Zhao YY, Li QY, Duan ZY, Tian LF, Chen Z, Lu JM, Liang XY, Zhao YF, Fu RG. Protective effects of GPR120 agonist-programmed macrophages on renal interstitial fibrosis in unilateral ureteral obstruction (UUO) rats. Biomedicine & Pharmacotherapy 2019, 117: 109172. PMID: 31261028, DOI: 10.1016/j.biopha.2019.109172.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsbeta CateninBiphenyl CompoundsCytokinesFibrosisGene Expression RegulationKidney DiseasesMacrophages, PeritonealMaleModels, BiologicalPhenotypePhenylpropionatesProtective AgentsRats, Sprague-DawleyReceptors, G-Protein-CoupledSignal TransductionTransforming Growth Factor beta1Ureteral ObstructionVimentinConceptsRenal interstitial fibrosisUnilateral ureteral obstructionInterstitial fibrosisUreteral obstructionProtective effectFree fatty acid receptor GPR120Fatty acid receptor GPR120Unilateral ureteral obstruction operationPeritoneal macrophagesAbnormal expressionExpression of CD206M2 phenotype macrophagesTumor necrosis factorEpithelial-mesenchymal transitionAutologous administrationReceptor GPR120UUO ratsInterleukin-6Intrarenal injectionArginase-1Necrosis factorGPR120 agonistM2 phenotypeΑ-SMATGF-β1
2018
Targeting the ErbB Family in Head and Neck Cancer
Kiseleva A, Beck T, Serebriiskii I, Liu H, Burtness B, Golemis E. Targeting the ErbB Family in Head and Neck Cancer. Current Cancer Research 2018, 7-61. DOI: 10.1007/978-3-319-78762-6_2.Peer-Reviewed Original ResearchPI3K/Akt/mTORSquamous cell carcinomaErbB receptor tyrosine kinase familyNovel therapeutic approachesAkt/mTORErbB family receptorsJAK1/STAT3PLC/PKCErbB family membersEGFR therapyCell carcinomaCommon therapyNeck cancerReceptor tyrosine kinase familyTherapeutic approachesNew therapiesCancer growthAbnormal expressionFamily receptorsTherapyTyrosine kinase familySCCHNErbB familyNormal cellsFamily members
2016
A Practical Approach to the Classification of WHO Grade 3 (G3) Well-differentiated Neuroendocrine Tumor (WD-NET) and Poorly Differentiated Neuroendocrine Carcinoma (PD-NEC) of the Pancreas
Tang L, Basturk O, Sue J, Klimstra D. A Practical Approach to the Classification of WHO Grade 3 (G3) Well-differentiated Neuroendocrine Tumor (WD-NET) and Poorly Differentiated Neuroendocrine Carcinoma (PD-NEC) of the Pancreas. The American Journal Of Surgical Pathology 2016, 40: 1192-1202. PMID: 27259015, PMCID: PMC4988129, DOI: 10.1097/pas.0000000000000662.Peer-Reviewed Original ResearchConceptsHigh-grade pancreatic neuroendocrine neoplasmsAbnormal expression of p53PD-NECsWD-NETsPancreatic neuroendocrine neoplasmsNeuroendocrine neoplasmsExpression of p53Loss of DAXXNeuroendocrine carcinomaPoor-differentiated neuroendocrine carcinomasHigh-grade neuroendocrine neoplasmsAccurate diagnosisEvaluate immunohistochemical stainingG3 neuroendocrine neoplasmsHigh-grade progressionWHO grade 3Hematoxylin and eosin sectionsDisease-specific survivalAbnormal expressionGroup of tumorsDegree of diagnostic concordanceWHO classification schemeATRX protein expressionCoexisting adenocarcinomaAbnormal p53
2015
Metabolic tumor burden is associated with major oncogenomic alterations and serum tumor markers in patients with resected pancreatic cancer
Shi S, Ji S, Qin Y, Xu J, Zhang B, Xu W, Liu J, Long J, Liu C, Liu L, Ni Q, Yu X. Metabolic tumor burden is associated with major oncogenomic alterations and serum tumor markers in patients with resected pancreatic cancer. Cancer Letters 2015, 360: 227-233. PMID: 25687883, DOI: 10.1016/j.canlet.2015.02.014.Peer-Reviewed Original ResearchConceptsMetabolic tumor burdenMetabolic tumor volumeSerum tumor markersTumor burdenTumor markersPancreatic cancerAbnormal expressions of TP53Abnormal expressionMonitoring treatment responsePancreatic cancer patientsProgression of pancreatic cancerExpression of TP53Tumor volumeCA19-9SMAD4/DPC4 geneTreatment responseCancer patientsDisease progressionPET/CTPredictive significanceSurvival rateLethal diseasePatientsCancerSerum
2014
MicroRNA and gynecological reproductive diseases
Santamaria X, Taylor H. MicroRNA and gynecological reproductive diseases. Fertility And Sterility 2014, 101: 1545-1551. PMID: 24882618, DOI: 10.1016/j.fertnstert.2014.04.044.Peer-Reviewed Original ResearchConceptsSmall non-coding RNAsTranslation of mRNAsNon-coding RNAsAberrant miRNA expressionHuman diseasesMiRNA expressionAbnormal expressionMicroRNAsReproductive tract diseaseReproductive diseasesExpressionGenesMiRNAsMiRNARNATranslationMRNATherapeutic toolDysregulationGynecological diseasesInflammatory diseases
2009
Towards Identification of Hereditary DNA Mismatch Repair Deficiency: Sebaceous Neoplasm Warrants Routine Immunohistochemical Screening Regardless of Patient's Age or Other Clinical Characteristics
Orta L, Klimstra D, Qin J, Mecca P, Tang L, Busam K, Shia J. Towards Identification of Hereditary DNA Mismatch Repair Deficiency: Sebaceous Neoplasm Warrants Routine Immunohistochemical Screening Regardless of Patient's Age or Other Clinical Characteristics. The American Journal Of Surgical Pathology 2009, 33: 934-944. PMID: 19342947, DOI: 10.1097/pas.0b013e318199edca.Peer-Reviewed Original ResearchConceptsTumor-infiltrating lymphocytesDNA mismatch repair deficiencyPeritumoral lymphocytic responseSebaceous neoplasmsMismatch repair deficiencyDNA mismatch repair proteinsPatient ageClinical characteristicsLymphocyte responsesAbnormal expressionSebaceous adenomaSebaceous tumorsRepair deficiencyMismatch repair proteinsImmunohistochemical expression of MLH1Head and neckPositive family historyAbnormal IHC stainingExpression of DNA mismatch repair proteinsIdentical staining patternStudy tissue samplesRepair proteinsSebaceous carcinomaVisceral malignancyTumor types
2006
Fire and phantoms after spinal cord injury: Na+ channels and central pain
Waxman S, Hains B. Fire and phantoms after spinal cord injury: Na+ channels and central pain. Trends In Neurosciences 2006, 29: 207-215. PMID: 16494954, DOI: 10.1016/j.tins.2006.02.003.Peer-Reviewed Original ResearchConceptsSpinal cord injuryNeuropathic painCord injurySpinal cord dorsal horn neuronsDorsal horn neuronsNervous system injuryCentral painPain pathwaysSystem injuryThalamic neuronsPainAbnormal expressionPhantom phenomenaNeuronsInjuryMolecular targetsMolecular changesRecent findingsHyperexcitabilityNav1.3Molecular basisCardiomyopathic Etiology and SERCA2a Reverse Remodeling During Mechanical Support of the Failing Human Heart
Heerdt PM, Klotz S, Burkhoff D. Cardiomyopathic Etiology and SERCA2a Reverse Remodeling During Mechanical Support of the Failing Human Heart. Anesthesia & Analgesia 2006, 102: 32-37. PMID: 16368801, DOI: 10.1213/01.ane.0000183642.09435.ad.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnalysis of VarianceAnimalsBiomechanical PhenomenaCalcium-Transporting ATPasesCardiomyopathy, DilatedConfidence IntervalsDatabases, FactualFemaleGene Expression Regulation, EnzymologicHeart-Assist DevicesHumansIn Vitro TechniquesMaleMiddle AgedRatsSarcoplasmic Reticulum Calcium-Transporting ATPasesVentricular RemodelingConceptsLeft ventricular assist deviceForce-frequency relationshipSERCA2a functionMyocardial force-frequency relationshipMyocyte calcium cyclingSERCA2a gene expressionFailing Human HeartVentricular assist deviceChronic failureProportion of trabeculaeReverse remodelingLVAD supportMyopathic originSubtype 2aDCM heartsDisease processSERCA2a mRNAAssist deviceCalcium cyclingHeart samplesAbnormal expressionMyocardial trabeculaeGene expressionMolecular remodelingHuman heart
2004
Tissue expression of transforming growth factor-β1 and its receptors: correlation with pathologic features and biochemical progression in patients undergoing radical prostatectomy
Shariat S, Menesses-Diaz A, Kim I, Muramoto M, Wheeler T, Slawin K. Tissue expression of transforming growth factor-β1 and its receptors: correlation with pathologic features and biochemical progression in patients undergoing radical prostatectomy. Urology 2004, 63: 1191-1197. PMID: 15183988, DOI: 10.1016/j.urology.2003.12.015.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedDisease ProgressionFollow-Up StudiesHumansImmunohistochemistryMaleMiddle AgedMultivariate AnalysisNeoplasm StagingProstateProstate-Specific AntigenProstatectomyProstatic HyperplasiaProstatic NeoplasmsReceptors, Transforming Growth Factor betaTransforming Growth Factor betaTransforming Growth Factor beta1ConceptsPlasma TGF-beta1 levelsTGF-beta1 levelsAbnormal expressionTGFbeta-RIITGFbeta-RIBiochemical progressionRadical prostatectomyProstate cancerPathologic Gleason scoreSeminal vesicle involvementSurgical margin statusProstate cancer featuresTissue expressionGrowth factor-β1TGF-beta1 overexpressionConsecutive patientsExtracapsular diseaseMargin statusPathologic featuresGleason scoreBlood levelsLoss of expressionPrognostic markerImmunohistochemical stainingFactor-β1
2001
Acquired channelopathies in nerve injury and MS
Waxman S. Acquired channelopathies in nerve injury and MS. Neurology 2001, 56: 1621-1627. PMID: 11428390, DOI: 10.1212/wnl.56.12.1621.Peer-Reviewed Original ResearchConceptsNerve injurySodium channelsSensory neuron-specific sodium channelsSodium channel geneChannel genesPeripheral nerve injurySpinal sensory neuronsPathophysiology of MSSubtype-specific drugsDistinct sodium channelsVoltage-gated sodium channelsSpecific sodium channelsAxonal transectionGenetic channelopathyPrototype disorderSensory neuronsPurkinje cellsTherapeutic opportunitiesChannelopathiesAbnormal expressionInjuryMolecular changesHyperexcitabilityCellsTransection
1999
The molecular pathophysiology of pain: abnormal expression of sodium channel genes and its contributions to hyperexcitability of primary sensory neurons
Waxman S. The molecular pathophysiology of pain: abnormal expression of sodium channel genes and its contributions to hyperexcitability of primary sensory neurons. Pain 1999, 82: s133-s140. PMID: 10491982, DOI: 10.1016/s0304-3959(99)00147-5.Peer-Reviewed Original ResearchConceptsPrimary sensory neuronsSodium channel gene expressionChannel gene expressionSodium channel expressionDRG neuronsSensory neuronsSodium channelsAxonal injuryChannel expressionSmall dorsal root ganglion neuronsAbnormal expressionDorsal root ganglion neuronsMolecular pathophysiologySodium channel geneAbnormal burst activityMultiple sodium channelsSNS/PN3Inflammatory pain modelChannel genesDistinct sodium channelsSodium current expressionInflammatory painNerve injuryPain modelGanglion neurons
1998
Endocytosis proteins and cancer: a potential link?
Floyd S, De Camilli P. Endocytosis proteins and cancer: a potential link? Trends In Cell Biology 1998, 8: 299-301. PMID: 9704404, DOI: 10.1016/s0962-8924(98)01316-6.Peer-Reviewed Original ResearchConceptsEndocytosis proteinsVariety of proteinsHuman haematopoietic malignanciesReceptor-mediated endocytosisAbnormal expressionClathrin adaptorsBiology of cancerChromosomal rearrangementsHuman cancersProteinHaematopoietic malignanciesRecent studiesPotential mechanismsExpressionPotential linkClathrinEndocytosisGenesAdaptorBiologyMutationsRearrangementCancerTarget
1988
Expression of messenger ribonucleic acids encoding a parathyroid hormone-like peptide in normal human and animal tissues with abnormal expression in human parathyroid adenomas.
Ikeda K, Weir E, Mangin M, Dannies P, Kinder B, Deftos L, Brown E, Broadus A. Expression of messenger ribonucleic acids encoding a parathyroid hormone-like peptide in normal human and animal tissues with abnormal expression in human parathyroid adenomas. Endocrinology 1988, 2: 1230-6. PMID: 3216862, DOI: 10.1210/mend-2-12-1230.Peer-Reviewed Original ResearchConceptsPTH-like peptideHuman parathyroid adenomasParathyroid adenomaAbnormal human parathyroid tissueHuman parathyroid tissueNumber of endocrineMedullary carcinoma cellsParathyroid hormone-like peptideExpression of mRNAAutonomous glandsHumoral hypercalcemiaParathyroid tissueHormone-like peptideAdrenal cortexRat brainNonendocrine tissuesAdrenal medullaBone marrowMessenger ribonucleic acidStomach mucosaHuman osteosarcomaOverexpression of transcriptsRat pituitaryNormal humansAbnormal expressionbFGF as an autocrine growth factor for human melanomas.
Halaban R, Kwon BS, Ghosh S, Delli Bovi P, Baird A. bFGF as an autocrine growth factor for human melanomas. Oncogene Research 1988, 3: 177-86. PMID: 3226725.Peer-Reviewed Original ResearchConceptsBasic fibroblast growth factorNormal human melanocytesBFGF gene transcriptsHuman melanocytesGrowth factorAutocrine growth factorGene transcriptsHuman metastatic melanomaMolecular mechanismsFibroblast growth factorNormal melanocytesCyclic adenosine monophosphateSerum-containing mediumAnti-bFGF antibodyMelanoma cellsAbnormal expressionAdenosine monophosphateHuman melanomaMelanocytesRegular culture mediumDibutyryl cyclic adenosine monophosphateMitogenic activityCulture mediumCellsTranscripts
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply