2022
Adaptive immune resistance at the tumour site: mechanisms and therapeutic opportunities
Kim TK, Vandsemb EN, Herbst RS, Chen L. Adaptive immune resistance at the tumour site: mechanisms and therapeutic opportunities. Nature Reviews Drug Discovery 2022, 21: 529-540. PMID: 35701637, DOI: 10.1038/s41573-022-00493-5.Peer-Reviewed Original ResearchConceptsAdaptive immune resistanceImmune resistanceCell death 1 ligand 1Tumor siteDeath 1 ligand 1Anti-PD therapyBlockade of PDL1Advanced-stage cancerFraction of patientsStrong mechanistic rationaleFuture drug developmentCurrent cancer therapiesImmune attackClinical trialsSolid tumorsTherapeutic opportunitiesTumorsCancer therapySelective inductionAntitumour drugsLigand 1Drug developmentTherapyAdditive effectMechanistic rationalePatterns of cardiometabolic multimorbidity and the risk of depressive symptoms in a longitudinal cohort of middle-aged and older Chinese
Huang ZT, Luo Y, Han L, Wang K, Yao SS, Su HX, Chen S, Cao GY, De Fries CM, Chen ZS, Xu HW, Hu YH, Xu B. Patterns of cardiometabolic multimorbidity and the risk of depressive symptoms in a longitudinal cohort of middle-aged and older Chinese. Journal Of Affective Disorders 2022, 301: 1-7. PMID: 34999125, DOI: 10.1016/j.jad.2022.01.030.Peer-Reviewed Original ResearchConceptsCardiometabolic multimorbidityCardiometabolic diseasesHeart diseaseDepressive symptomsSelf-reported chronic conditionsEpidemiological Studies Depression ScaleAbsence of strokeRisk of depressionRetirement Longitudinal Study 2011Multiple cardiometabolic diseasesDose effectMental health preventionOlder ChineseAdditive effectChronic conditionsDisease combinationsLongitudinal cohortDepression ScaleHigh riskMultimorbidityPerson-centered healthcareDiabetesSymptomsHealth preventionChina Health
2021
Child Maltreatment, Peer Victimization, and Mental Health: Neurocognitive Perspectives on the Cycle of Victimization
Goemans A, Viding E, McCrory E. Child Maltreatment, Peer Victimization, and Mental Health: Neurocognitive Perspectives on the Cycle of Victimization. Trauma Violence & Abuse 2021, 24: 530-548. PMID: 34355601, PMCID: PMC10009486, DOI: 10.1177/15248380211036393.Peer-Reviewed Original ResearchConceptsMental healthMental health careMental health outcomesAdverse childhood experiencesMental health vulnerabilitiesSystematic scoping reviewInpatient populationChild maltreatmentHealth outcomesGoogle ScholarHealth careNeurocognitive functioningPutative mechanismsRisk of revictimizationScoping ReviewHealth vulnerabilityChildrenNeurocognitive findingsPreventative modelAdditive effectChildhood experiencesRiskPeer victimizationHealthMaltreatment
2020
Induced pluripotent stem cell reprogramming‐associated methylation at the GABRA2 promoter and chr4p12 GABAA subunit gene expression in the context of alcohol use disorder
Goetjen A, Watson M, Lieberman R, Clinton K, Kranzler H, Covault J. Induced pluripotent stem cell reprogramming‐associated methylation at the GABRA2 promoter and chr4p12 GABAA subunit gene expression in the context of alcohol use disorder. American Journal Of Medical Genetics Part B Neuropsychiatric Genetics 2020, 183: 464-474. PMID: 33029895, PMCID: PMC8022112, DOI: 10.1002/ajmg.b.32824.Peer-Reviewed Original ResearchConceptsGene expressionSubunit gene expressionSubunit geneNeural culturesInduced pluripotent stem cellsReceptor subunit genesPluripotent stem cellsStochastic methylationGene clusterDNA methylationCpG methylationMethylation levelsReceptor subunit gene expressionMethylationSignificant genetic contributionGenesStem cellsGenetic contributionMolecular effectsIPSC linesGABRB1 geneExpressionGABRA2GenotypesAdditive effectGlobal Profiling of Cellular Substrates of Human Dcp2
Luo Y, Schofield J, Simon MD, Slavoff SA. Global Profiling of Cellular Substrates of Human Dcp2. Biochemistry 2020, 59: 4176-4188. PMID: 32365300, PMCID: PMC7641959, DOI: 10.1021/acs.biochem.0c00069.Peer-Reviewed Original ResearchConceptsDecapping enzymeFirst committed stepCellular transcriptsP-bodiesRNA decayCommitted stepHuman transcriptomeMammalian cellsMolecular marksKnockout cellsGlobal profilingConsensus sequenceCellular substratesDCP2Human cellsTranscriptsEnzymeEnzyme substrateCellsDistinct subsetsTranscriptomeAdditive effectEnrichmentRNACytoplasm
2019
Revisiting the non-Gaucher-GBA-E326K carrier state: Is it sufficient to increase Parkinson's disease risk?
Goldstein O, Gana-Weisz M, Cohen-Avinoam D, Shiner T, Thaler A, Cedarbaum JM, John S, Lalioti M, Gurevich T, Bar-Shira A, Mirelman A, Giladi N, Orr-Urtreger A. Revisiting the non-Gaucher-GBA-E326K carrier state: Is it sufficient to increase Parkinson's disease risk? Molecular Genetics And Metabolism 2019, 128: 470-475. PMID: 31662221, DOI: 10.1016/j.ymgme.2019.10.001.Peer-Reviewed Original ResearchConceptsPD patientsE326KGBA variantsLRRK2 G2019SDisease riskDisease worldElderly healthy individualsAdditive effectParkinson's disease riskK variantAshkenazi PD patientsCommon genetic risk factorGenetic risk factorsRisk factorsCarrier patientsGBA mutationsPD riskHealthy individualsPatientsCarrier stateGaucher diseaseEarlier AAOAshkenazi originAshkenazi controlsStatistical significanceDetermining the endocrine disruption potential of industrial chemicals using an integrative approach: Public databases, in vitro exposure, and modeling receptor interactions
Alofe O, Kisanga E, Inayat-Hussain SH, Fukumura M, Garcia-Milian R, Perera L, Vasiliou V, Whirledge S. Determining the endocrine disruption potential of industrial chemicals using an integrative approach: Public databases, in vitro exposure, and modeling receptor interactions. Environment International 2019, 131: 104969. PMID: 31310931, PMCID: PMC6728168, DOI: 10.1016/j.envint.2019.104969.Peer-Reviewed Original ResearchConceptsEstrogen receptorEstradiol-mediated inductionLow-dose combinationIshikawa cell lineLow-dose effectsDirect stimulatoryPotential of chemicalsRate of proliferationOccupational exposureIshikawa cellsAnimal modelsHuman studiesReproductive toxicityCarcinogenic effectsInhibitory effectToxicology testingEndocrineCell proliferationEndocrine disruption potentialDose effectReceptor interactionIndustrial chemicalsCell linesPublic healthAdditive effect
2018
Low-Frequency and Rare-Coding Variation Contributes to Multiple Sclerosis Risk
Consortium I, Mitrovič M, Patsopoulos N, Beecham A, Dankowski T, Goris A, Dubois B, D’hooghe M, Lemmens R, Van Damme P, Søndergaard H, Sellebjerg F, Sorensen P, Ullum H, Thørner L, Werge T, Saarela J, Cournu-Rebeix I, Damotte V, Fontaine B, Guillot-Noel L, Lathrop M, Vukusik S, Gourraud P, Andlauer T, Pongratz V, Buck D, Gasperi C, Bayas A, Heesen C, Kümpfel T, Linker R, Paul F, Stangel M, Tackenberg B, Bergh F, Warnke C, Wiendl H, Wildemann B, Zettl U, Ziemann U, Tumani H, Gold R, Grummel V, Hemmer B, Knier B, Lill C, Luessi F, Dardiotis E, Agliardi C, Barizzone N, Mascia E, Bernardinelli L, Comi G, Cusi D, Esposito F, Ferrè L, Comi C, Galimberti D, Leone M, Sorosina M, Mescheriakova J, Hintzen R, van Duijn C, Theunissen C, Bos S, Myhr K, Celius E, Lie B, Spurkland A, Comabella M, Montalban X, Alfredsson L, Stridh P, Hillert J, Jagodic M, Piehl F, Jelčić I, Martin R, Sospedra M, Ban M, Hawkins C, Hysi P, Kalra S, Karpe F, Khadake J, Lachance G, Neville M, Santaniello A, Caillier S, Calabresi P, Cree B, Cross A, Davis M, Haines J, de Bakker P, Delgado S, Dembele M, Edwards K, Fitzgerald K, Hakonarson H, Konidari I, Lathi E, Manrique C, Pericak-Vance M, Piccio L, Schaefer C, McCabe C, Weiner H, Goldstein J, Olsson T, Hadjigeorgiou G, Taylor B, Tajouri L, Charlesworth J, Booth D, Harbo H, Ivinson A, Hauser S, Compston A, Stewart G, Zipp F, Barcellos L, Baranzini S, Martinelli-Boneschi F, D’Alfonso S, Ziegler A, Oturai A, McCauley J, Sawcer S, Oksenberg J, De Jager P, Kockum I, Hafler D, Cotsapas C. Low-Frequency and Rare-Coding Variation Contributes to Multiple Sclerosis Risk. Cell 2018, 175: 1679-1687.e7. PMID: 30343897, PMCID: PMC6269166, DOI: 10.1016/j.cell.2018.09.049.Peer-Reviewed Original ResearchConceptsRare coding variationsGenome-wide association studiesNon-coding variationCommon variant signalsSubstantial linkage disequilibriumLow-frequency variantsNovel genesCell homeostasisAssociation studiesComplex neurological diseasesLinkage disequilibriumGenetic variantsCommon variantsHeritabilityRich resourceGenesVariantsKey pathogenic roleIndividual familiesEpistasisAdditive effectBiologyHomeostasisMutationsNeurological diseasesNormal angulation of skull base in Apert syndrome
Lu X, Forte AJ, Sawh-Martinez R, Wu R, Cabrejo R, Steinbacher DM, Alperovich M, Alonso N, Persing JA. Normal angulation of skull base in Apert syndrome. Journal Of Cranio-Maxillofacial Surgery 2018, 46: 2042-2051. PMID: 30391086, DOI: 10.1016/j.jcms.2018.09.026.Peer-Reviewed Original ResearchConceptsAnterior cranial baseApert syndromeCranial base lengthSkull baseSevere craniofacial deformitiesPosterior cranial base lengthYears of ageMonths of ageUnoperated patientsCT scanAnterior cranial base lengthCranial base angleLate infancySyndromeAge rangeCraniofacial deformitiesCranial baseDeformityAdditive effectSkull vaultMonthsAngulationSignificant changesAgeBase length
2015
Contributions of Comorbid Diabetes to Sleep Characteristics, Daytime Symptoms, and Physical Function Among Patients With Stable Heart Failure
Fritschi C, Redeker NS. Contributions of Comorbid Diabetes to Sleep Characteristics, Daytime Symptoms, and Physical Function Among Patients With Stable Heart Failure. The Journal Of Cardiovascular Nursing 2015, 30: 411-419. PMID: 25078876, PMCID: PMC4312262, DOI: 10.1097/jcn.0000000000000183.Peer-Reviewed Original ResearchConceptsStable heart failureDiabetes mellitusHeart failurePoor physical functioningHF patientsDaytime symptomsPhysical functionSleep disturbancesPhysical functioningSleep characteristicsSleep qualityNew York Heart Association classNew York Heart Association classificationSelf-reported physical functionPhysical component summary scoreSelf-reported sleep qualityComorbid diabetes mellitusRespiratory disturbance indexComponent summary scoresMedical Outcomes StudySleep-disordered breathingBody mass indexPhysical function measuresAdditive effectLower general health
2014
Cigarette smoking worsens systemic inflammation in persons with metabolic syndrome
Jamal O, Aneni EC, Shaharyar S, Ali SS, Parris D, McEvoy JW, Veledar E, Blaha MJ, Blumenthal RS, Agatston AS, Conceição RD, Feldman T, Carvalho JA, Santos RD, Nasir K. Cigarette smoking worsens systemic inflammation in persons with metabolic syndrome. Diabetology & Metabolic Syndrome 2014, 6: 79. PMID: 25960769, PMCID: PMC4424791, DOI: 10.1186/1758-5996-6-79.Peer-Reviewed Original ResearchHs-CRPSystemic inflammationCigarette smokingMetabolic syndromeHigh-sensitivity C-reactive proteinCardiovascular disease riskC-reactive proteinCombination of smokingLogistic regression modelsBackgroundEmerging dataSmoking statusSmoking cessationReactive proteinEntire populationSmokersSmokingInflammationDisease riskBrazilian subjectsMetSRegression analysisSignificant increaseSyndromeRiskAdditive effect
2013
Evidence-Based Cardiovascular Management of Patients Receiving Radiotherapy to the Heart
Taylor B, Evans S, Roberts K. Evidence-Based Cardiovascular Management of Patients Receiving Radiotherapy to the Heart. 2013, 409-420. DOI: 10.1007/978-1-4471-4441-0_28.ChaptersCardiovascular managementLong-term outcome studiesLate cardiovascular complicationsPrimary care physiciansEffect of radiotherapyRisks of radiotherapyCardiovascular complicationsCardiotoxic chemotherapyCare physiciansCardiovascular functionOutcome studiesCardiovascular teamRT planningRadiotherapyCardiovascular systemPatientsCancer therapyTherapy techniquesCell populationsAdverse changesChemotherapyHeartAdditive effectRiskTreatment
2012
The Carbon Monoxide Releasing Molecule CORM-2 Attenuates Pseudomonas aeruginosa Biofilm Formation
Murray TS, Okegbe C, Gao Y, Kazmierczak BI, Motterlini R, Dietrich LE, Bruscia EM. The Carbon Monoxide Releasing Molecule CORM-2 Attenuates Pseudomonas aeruginosa Biofilm Formation. PLOS ONE 2012, 7: e35499. PMID: 22563385, PMCID: PMC3338523, DOI: 10.1371/journal.pone.0035499.Peer-Reviewed Original ResearchConceptsCORM-2 treatmentP. aeruginosa lung infectionP. aeruginosaAeruginosa lung infectionCORM-2Clinical P. aeruginosaMolecule CORM-2Current antimicrobial agentsChronic infectionLung infectionNew therapiesRelated infectionsNon-mucoid strainsReactive oxygen speciesInfectionNovel therapeutic propertiesTherapeutic propertiesAntimicrobial agentsAdditive effectPseudomonas aeruginosaBiofilm formationOxygen speciesTreatmentAeruginosaA method for partitioning the attributable fraction of multiple time-dependent coexisting risk factors for an adverse health outcome.
Lin H, Allore HG, McAvay G, Tinetti ME, Gill TM, Gross CP, Murphy TE. A method for partitioning the attributable fraction of multiple time-dependent coexisting risk factors for an adverse health outcome. American Journal Of Public Health 2012, 103: 177-82. PMID: 22515873, PMCID: PMC3518339, DOI: 10.2105/ajph.2011.300458.Peer-Reviewed Original ResearchConceptsHealth outcomesAttributable fraction methodPrecipitating Events ProjectAdverse health outcomesMultiple diseasesAcute episodeNew onsetHeart failureAdverse outcomesRisk factorsAttributable fractionNew Haven CountyDiseaseIndividual diseasesOlder adultsOutcomesAdditive effectDeathEvent outcomesOnsetPneumoniaCohort
2010
Chemoprevention of Head and Neck Cancer with Green Tea Polyphenols
Kim JW, Amin AR, Shin DM. Chemoprevention of Head and Neck Cancer with Green Tea Polyphenols. Cancer Prevention Research 2010, 3: 900-909. PMID: 20663981, PMCID: PMC2917478, DOI: 10.1158/1940-6207.capr-09-0131.Peer-Reviewed Original ResearchConceptsSquamous cell carcinomaGreen tea polyphenolsCell carcinomaNovel clinical trial designsTea polyphenolsChemoprevention of headHigh-risk patientsKey molecular signaling pathwaysClinical trial designNatural dietary compoundsUse of biomarkersMolecular signaling pathwaysNeck cancerChemoprevention researchChemopreventive agentsDietary compoundsTrial designCarcinomaChemopreventionSignaling pathwaysAdditive effectNatural compoundsEGCGMajor advancesPolyphenols
2009
Eszopiclone and fluoxetine enhance the survival of newborn neurons in the adult rat hippocampus
Su XW, Li XY, Banasr M, Duman RS. Eszopiclone and fluoxetine enhance the survival of newborn neurons in the adult rat hippocampus. The International Journal Of Neuropsychopharmacology 2009, 12: 1421-1428. PMID: 19775501, PMCID: PMC3677220, DOI: 10.1017/s1461145709990629.Peer-Reviewed Original ResearchConceptsNewborn neuronsAntidepressant actionSerotonin uptake inhibitorAdult rat hippocampusAdult hippocampusCombined administrationDorsal hippocampusRat hippocampusPreclinical studiesAdult ratsUptake inhibitorFluoxetineHippocampusNewborn cellsClinical researchEszopicloneBehavioral actionsNeuronsSurvivalAdditive effectNovel mechanismProliferationAntidepressantsPatientsChronic
2008
Centralized Oversight of Physician–Scientist Faculty Development at Vanderbilt: Early Outcomes
Brown AM, Morrow JD, Limbird LE, Byrne DW, Gabbe SG, Balser JR, Brown NJ. Centralized Oversight of Physician–Scientist Faculty Development at Vanderbilt: Early Outcomes. Academic Medicine 2008, 83: 969-975. PMID: 18820531, PMCID: PMC3780596, DOI: 10.1097/acm.0b013e3181850950.Peer-Reviewed Original ResearchConceptsEarly outcomesYounger ageComparison cohortNational ratesNational InstituteK awardsOutcomesAdditive effect
2007
Crosstalk between VEGF-A/VEGFR2 and GDNF/RET signaling pathways
Tufro A, Teichman J, Banu N, Villegas G. Crosstalk between VEGF-A/VEGFR2 and GDNF/RET signaling pathways. Biochemical And Biophysical Research Communications 2007, 358: 410-416. PMID: 17490619, DOI: 10.1016/j.bbrc.2007.04.146.Peer-Reviewed Original ResearchConceptsVascular endothelial growth factorCell proliferationEndothelial growth factorNeurotrophic factorGDNF/RETEmbryonic kidney explantsUreteric bud branchingUreteric bud cellsC-RetGrowth factorRT-PCRVEGFNovel cooperative interactionVEGFR2Branching morphogenesisRETVEGFR2 autophosphorylationGDNFKidney developmentBud cellsUreteric budAdditive effectMajor regulatorKidney explantsPhosphorylation
2003
Two Distinct Phosphorylation Pathways Have Additive Effects on Abl Family Kinase Activation
Tanis KQ, Veach D, Duewel HS, Bornmann WG, Koleske AJ. Two Distinct Phosphorylation Pathways Have Additive Effects on Abl Family Kinase Activation. Molecular And Cellular Biology 2003, 23: 3884-3896. PMID: 12748290, PMCID: PMC155218, DOI: 10.1128/mcb.23.11.3884-3896.2003.Peer-Reviewed Original ResearchConceptsSrc nonreceptor tyrosine kinaseAdditive effectTyrosine kinaseArg nonreceptor tyrosine kinaseKinase activationNonreceptor tyrosine kinaseKinase activityCell surface receptorsSurface receptorsStimuli resultsStimulationFivefold stimulationActivationTwofold stimulationABLPhosphorylationPhosphorylation pathwayPathwaySrc family kinase HckSrc familyDesipramine and contingency management for cocaine and opiate dependence in buprenorphine maintained patients
Kosten T, Oliveto A, Feingold A, Poling J, Sevarino K, McCance-Katz E, Stine S, Gonzalez G, Gonsai K. Desipramine and contingency management for cocaine and opiate dependence in buprenorphine maintained patients. Drug And Alcohol Dependence 2003, 70: 315-325. PMID: 12757969, DOI: 10.1016/s0376-8716(03)00032-2.Peer-Reviewed Original ResearchConceptsCocaine-free urinesContingency managementCocaine useOpioid withdrawal symptomsUrine toxicology resultsDrug-free urineMethadone treatmentPoor prognosisWithdrawal symptomsMethadone maintenancePlasma levelsDependent patientsToxicology resultsTreatment groupsCell trialsCocaine abuseBuprenorphineDesipraminePatientsCocaine abusersOpiatesSymptom levelsUrineAdditive effectCocaine
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