UNIVERSITYOFMINNESOTA

2017SUMMERUNDERGRADUATERESEARCHSYMPOSIUM

LifeSciencesSummerUndergraduateResearchProgram

(LSSURP)

FacultyDirector:Dr.ColinCampbell

AdministrativeDirector:Dr.JonGottesman

ProgramCoordinator:EvelynJuliussen

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Presenter: NohaAbdelrahmanPosterNumber: 1HomeInstitution: NorthDakotaStateUniversityProgram: LSSURPFacultyMentor: Dr.LouisManskyResearchAdvisor: LuizaM.Mendonça,RuthBlower,JoséO.Maldonado,ShengCao,WeiZhangPosterTitle: InvestigationOfTheAcidicCarboxyl-TerminalRegionOfTheHTLV-1

Nucleocapsid(NC)DomainOfGagOnVirusParticleSizeAndCellularDistribution

Abstract: HumanT-cellleukemiavirustype1(HTLV-1)isacancer-causinghumanretrovirusthatinfectsabout15millionindividualsworldwide.ManyoftheaspectsofHTLV-1replication,includingvirusparticlestructureandassembly,arepoorlyunderstood.Group-specificantigen(Gag)proteinisthemajorretroviralstructuralproteinthatdrivesvirusparticleassembly.PreliminarystudiesbytheManskyresearchgrouphavesuggestedapotentialroleofthecarboxy(C)-terminalregion(whichisenrichedinacidicaminoacids)inthenucleocapsiddomainofGagonHTLV-1assembly.Basedupontheseobservations,ItestedthehypothesisthatdeletionofthisregionwouldinfluenceHTLV-1particleassembly.Specifically,IanalyzedseveralGagexpressionconstructs,whenintroducedintohumancells in culture result in the production of HTLV-1-like particles. First, I analyzed the cellulardistributionoftheGagproteinsbylaserscanningconfocalmicroscopy.Second,Ianalyzedthesizeand morphology of particles by cryo-transmission electron microscopy. My analyses havesuggestedthattheGagC-terminusdoesnotsignificantlyimpacttheformationofGagpunctabutdoes impact particle size and morphology. These observations help to lay the foundation forsubsequentstudies,andcontributetothelong-termobjectiveofunderstandinghowparticlesizeandmorphologyimpactsvirusinfectivity.

Presenter: SaadAbdulkadirPosterNumber: 2HomeInstitution: NormandaleCommunityCollegeProgram: LSSURPFacultyMentor: Dr.WenshengLinPosterTitle: TheEffectsofActivationTranscriptionFactor4ontheLowerMotorNeuron

andAxonslossinPatientwithMultipleSclerosisAbstract: UnfoldingProteinResponse(UPR)occursinresponsetoEndoplasmicReticulum(ER)stresscaused

byabuildupofunfoldedormisfoldedproteinsintheER.RecentstudieshaveshownupregulatedcomponentsofUPRinMultipleSclerosis(MS)lesions.PancreaticEndoplasmicReticulumKinase(PERK)isERtransmembraneproteinsthat’sbeenidentifiedastransducersofUPR.PreviousresearchhasshownOligodendrocyte-SpecificActivationofPERKsignalingattenuatesOligodendrocytedeathanddemyelination.InthisexperimentwehopedtodeterminethesignificanceofActivationTranscriptionProtein4(ATF4),oneofthethreemajordownstreampathwaysofPERK.TotestthesignificanceofATF4,webredourmicetocreateanAFT4knockoutmiceandwildtypemicewithAFT4.Weobservedbothgroupstoestablishthereisnosignificantdifference.AfterestablishtheremovalofAFT4doesnotaffectthehealthymiceinitiatetheExperimentalAutoimmuneEncephalomyelitis(EAE)mousemodeltosimulateMSinthemice.Themicearecloselyobservedforthenexttwentydays.Wedocumentedthebehaviorofmiceandclinicalscoresofthemice.Onthetwentyfirstdaythemicearescarifiedandperfusedforustocollecttissuesamplesandgraymatterfromthebrainandspinalcord.Usingimmunohistochemistry,wecomparethenumberofupperandlowermotorneurons,Purkinjecells,oligodendrocytes,andaxons.Althoughnotconclusive,ourinitialresultsareshowingATF4isnotsignificantintheattenuationofOligodendrocytedeathanddemyelination.WhenweconcludetheinsignificanceofAFT4,weplantomoveontothenextdownstreampathwayofPERKandtestitssignificance.

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Presenter: PaigeAkinsPosterNumber: 3HomeInstitution: UniversityofArkansas-PineBluffProgram: LSSURPFacultyMentor: Dr.MaryRogersPosterTitle: EffectsofLowTunnelPlasticTypeonEarlyDevelopmentofDay-Neutral

StrawberriesAbstract: StrawberryconsumptionintheU.S.issteadilyincreasing,anddemandisstrong

forlocallyproducedandorganicfruit.Protectedculturesystems,includinglowtunnels,modifythemicroclimateandallowforseasonextensionandhigherqualityfruit.Inthisproject,weinvestigatedtheeffectsofUVblockingandUVtransmittingplasticonearlygrowthofday-neutralstrawberriesinlowtunnels.Thisresearchprojectisbeingconductedwithinthecontextofalonger-termprojectlookingathowlowtunnelcoveringsaffectstrawberryfruityield,qualityandinsectpestmanagement.Inthisproject,weassessedvegetativeandreproductivegrowthandleafchlorophyllcontentofdayneutral‘Albion’strawberryplantsduringeightweeksofproductionunderthethreedifferenttreatments:UVtransmitting,UVblocking,andopenplots.Thetransmittingandblockingplastictreatmentssawsignificantlyhighernumbersofflowersandleavescomparedtotheopencontrolplots.Vegetativegrowthwasnotdistinctlycorrelatedwithleafchlorophyllcontentinanytreatments.TheseresearcheffortscontributetoourunderstandingofstrawberryproductioninMinnesotatohelpmeetthegrowingdemandsforlocal,organicstrawberries.

Presenter: JacqelineAldacoPosterNumber: 4HomeInstitution: BrynMawrCollegeProgram: LSSURPFacultyMentor: Dr.SylvainLesnéPosterTitle: QuantitationofGlialCellsintheProximityofAmyloidPlaquesAbstract: TheneurodegenerativedisorderAlzheimer’sdisease(AD)ischaracterizedby

amyloidplaques,neurofibrillarytangles,andneuronalloss.Amyloidplaquesoriginatefromtheamyloidogenicprocessingofitsprecursorprotein,APP,whichleadstotheaccumulationofbeta-amyloid(Aβ)peptides.Thecloseproximityoftheseplaquesareassociatedwithincreasedlevelsofsynapticlossanddystrophicneurites.Werecentlyobservedthatoverexpressingalpha-synucleininAPPmiceloweredamyloidburdenintheseanimalsbutsurprisinglyalsoworsenedcognition.Inthisstudy,wewereinterestedindeterminingwhetherthedensityofglialcells(i.e.astrocytesandmicroglia)changesdifferentiallybetweentheimmediatevicinityoftheplaquecore,thesurroundingtoxichalo.

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Presenter: MariaAnayaPosterNumber: 5HomeInstitution: StonyBrookStateUniversityProgram: LSSURPFacultyMentor: Dr.MichaelGeorgieffResearchAdvisor: AmandaBarks,PhuTranPosterTitle: InVitroAssessmentOfIron-DeficiencyInducedEpigeneticModificationsAt

TheBDNFPromoterInNeuronalCellsAbstract: Irondeficiency(ID)isthemostcommonnutritionaldeficiencythroughouttheworld.

Early-lifeIDhaslongtermeffects,includingreducedcognitivefunctionandincreasedriskofdepression,schizophreniaandautisminadulthood.Brain-derivedneurotrophicfactor(BDNF)isbroadlyexpressedindevelopingandadultmammalianbrainsandisessentialinneuronaldifferentiation,proliferation,andsynapticplasticity.Inanimalmodelsofearly-lifeID,BdnfgeneexpressionisdownregulatedduringandbeyondtheIDperiod.Bdnfisepigeneticallymodifiable.JARID-mediatedhistonedemethylationisaknowniron-dependentepigeneticmodificationthatmayexplainthelong-termeffectsofIDonBDNFexpression.WehypothesizethatalteredJARID-mediatedhistonemethylationisamechanismbywhichIDinduceslong-termBdnfdysregulation.IDwillbeinducedinimmortalizedhippocampalneurons(HT-22)usingdeferoxamine(DFO),anironchelator.ExpressionofBdnfandtransferrinreceptor(TfRc)willbequantifiedbyqPCR.Levelsofhistonemethylation(K4me3)andJARID1b(K4me3demethylase)bindingattheBdnf-IVpromoterwillbequantifiedbyChIP-qPCR.Inaddition,HT-22cellswillbetreatedwithPBIT,aJARID1Binhibitor,todeterminewhetherJARID1BmediatethedecreaseinBdnfexpressionfollowingID.Preliminarydatashoweda3-foldincreaseinTfRcexpression,indicatingthatIDwasinduced,accompaniedbya50%decreaseinBdnfexpression,whencellsaretreatedwith25uMDFOfor24hours.

Presenter: MichaelAndersonPosterNumber: 6HomeInstitution: UniversityofNotreDameProgram: LSSURPFacultyMentor: Dr.BryceBinstadtResearchAdvisor: NathanSchuldtPosterTitle: GenerationofaMousetoTrackDualTCRTCellsAbstract: ThymicselectionshapestheTcellreceptor(TCR)repertoirebydeletingpotentially

harmfulTCRs.Despitethisessentialroleinimmunity,thymicselectionremainsincompletelyunderstood.LeadingtheoriesonthymicselectionassumethataTcellexpressesonlyoneTCRspecificity.However,currentevidenceestimatesbetween10and30percentofTcellsexpressafunctionallyrecombinedTCRfrombothalleles.AdvancementsinthisareaofresearchhavebeenlimitedbythelackofavailablereagentstoreliablydetectthesedualTCRTcells.Inordertoaddressthisgapinknowledge,weareengineeringadualTCRTcellreportermousethatwillallowustodetect,enumerate,andtrackdualTCRTcells.WegeneratedtwodifferentstrainsofTCRreportermice,eachwithauniquesmallepitopetagattachedtotheTCRαconstantregionsharedbyallTCRsrecombinedfromthatallele.Oncebredtogether,wewillbeabletodetectcellsthatexpressTCRsrecombinedfrombothallele(i.e.dualTCRTcells)usingflowcytometricanalysiswithfluorescentlylabeledantibodiesspecificforthetwosmallepitopetags.ThisexcitingnewtoolwillallowustodesignnovelexperimentstostudytheeffectofdualTCRTcellsonthymicselectionandimmunity.HereIfocusonoptimizingdetectionofthereportertaginthesemice.

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Presenter: WilliamAndersonPosterNumber: 7HomeInstitution: MacalesterCollegeProgram: LSSURPFacultyMentor: Dr.MarkSchleissPosterTitle: DeterminingAntibodyResponseToSectionsOfGP129,GP133,AndgL

(GP115)OfThePentamericComplexInGuineaPigCytomegalovirusAbstract: Cytomegalovirus(CMV)istheleadingviralcauseofbirthdefectsintheworld.

Thepentamericcomplexisa5-proteincomplexthatisnecessaryforvirusentryintoepithelialandendothelialcellsandhasbecomeapointofinterestinvaccinationefforts.GuineaPigsareausefulmodelofhumanCMV(HCMV)infectionsincethemodeoftrans-placentaltransmissionissimilartothatinhumans.UsingGuineaPigCMV(GPCMV)asamodel,weselectedsectionsofthepentamericproteinsGP129,GP133andgL(GP115)tobeconjugatedintoacarrierproteinandthentheseconjugateswereintroducedintorabbitstoelicitapolyclonalantibodyresponse.Usingthegeneratedantibodies,weperformedELISAstodeterminetheantibody’stiteragainsttheboththepeptideitwasmadetoandtoviralparticlesofGPCMV.Wealsocompletedwesternblottingassaystodetermineantibodyspecificitytoviralparticles.Weaimtodeterminewhichareasoftheseproteinscanbetargetedeffectivelybygeneratedantibodies.OurresultswillfurtherunderstandingofthenaturalantibodyresponsetoCMVandpossiblyaidinthedevelopmentofavaccineorbetterscreeningforHCMV.

Presenter: EvanBanksPosterNumber: 8HomeInstitution: UniversityofMinnesota-TwinCitiesProgram: LSSURPFacultyMentor: Dr.JonathanGewirtzResearchAdvisor: XinSongPosterTitle: ClassicalConditioningofanOdorPreferenceinMiceAbstract: ConditionedOdorPreference(COP)isarecentlydevelopedclassical

conditioningtechniquethatcanmeasureaddictivebehaviorinrodentsbytesting.ThepurposeofthisstudywastouseCOPasanewparadigmtotestwhethermicedevelopapositiveassociationbetweenadrugstateandaneutralodor.Inthepresentstudy,wild-typewerefirstsubjectedtoapretestthatmeasuredwhethertheyprefervanillaoralmondsscents.Duringtheconditioningphase,theywereweighedandinjectedwith0.2-0.35mlofeithersalineormorphineonalternatedaysfor8days.Afterinjection,themice’sodorpreferencewasmeasuredintheCOPparadigm.OdorpreferencewasquantifiedusingAnimaze,tomeasurethemouse’stimeinvestigatingeachscent.Longerinvestigationindicatedhigherpreference.Wefoundthatmiceonmorphinedonotinvestigateeitherscenttoasignificantlyhigherdegreethanthesalinegroup,indicatingthattheydidnotdevelopapositiveassociationbetweenadrugstateandaneutralodor.Theseresultsdonotsupportpreviousstudiesthatindicatethatmiceinamorphine-inducedstatedevelopaclassicallyconditionedpreferenceforpreviouslyneutralodor.

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Presenter: SocratesBassukPosterNumber: 9HomeInstitution: OberlinCollegeProgram: LSSURPFacultyMentor: Dr.ChangbinChenPosterTitle: ASearchforanATMGeneMutationinMaizeAbstract: TheAtaxiatelangiectasiamutated(ATM)isahighlyconservedeukaryoticgene

crucialforDNAdouble-strandbreaksthatoccurduringmeiosisaswellasthoseinducedbyDNAdamagingagents.Ithasbeenwell-characterizedinmammalsduetoitsroleincancer.Inplantshowever,understandingofATMisvirtuallylimitedtoArabidopsisradiationresponse.WeconductedasearchforanATMmutationinmaize,aneconomicallyimportantcropwithabiggergenomeandmorerepetitiveDNAcontentthanArabidopsis.BasedontheArabidopsisATMgene,weidentifiedthehomologinmaizeandsearchedforavailablemutants.Usingpolymerasechainreaction(PCR),weidentifiedoneputativemutantwithaMutransposoninsertioninapredictedintron-exonboundary.PlantshomozygousfortheMutransposoninsertiondidnotshowanyobviousvegetativegrowthphenotypes.PlantsthatareeitherheterozygousorhomozygousfortheMuinsertionwerefoundlessthanexpectedbasedonMendeliansegregation,indicatingthatreproductivecelldevelopmentmightbeaffected.Pollenfertilitytestswillbeconductedtodeterminethefertilitystatusofthedifferentgenotypes.TheunderstandingofATM’sroleinmaizemeiosiswillextendourknowledgeofthefunctionofthisgeneinplants.

Presenter: DannyBaumannPosterNumber: 10HomeInstitution: MacalesterCollegeProgram: LSSURPFacultyMentor: Dr.RobertKratzkePosterTitle: Immunogeniccelldeathinducedviavirotherapyandruxolitinibtreatmentin

non-smallcelllungcancerAbstract: Non-smallcelllungcarcinoma(NSCLC)isaformofepitheliallungcancerthat

accountsfor85%ofalllungcancers.NSCLCisresistanttochemotherapy,butimmunotherapyhasbeenshowntobeaneffectivetreatment.Previousstudieshaveshownthatthevesicularstomatitisvirus(VSV),thatproducesinterferonβ(VSV-IFNβ)canenhancethebody'simmuneresponsetoNSCLCthereforeitishypothesizedthatthemechanisminvolvesimmunogeniccelldeath(ICD).ICDischaracterizedbythesecretionofDAMPs(dangerassociatedmolecularpatterns)thatoperateonaseriesofreceptorsexpressedbythedendriticcells.OnceactivatedbytheDAMPsthedendriticcelldeliverstheantigentotheT-cellinordertokillcancer.LM2andLLCmousecelllinesweretreatedwithvariousconcentrationsofVSV-IFNβandRuxolitinibinordertovisualizetheroutethatinducesICD.Killcurvesweregeneratedaftera72hourtreatmentandDAMPexpressionwasmeasuredemployingELISAtoquantifytheICDresponsecausedbyVSV-IFNβtreatment.ToassesstheintegrityoftheJAK/STATpathwayaspartoftheinterferonresponse,immunoblotswererunonSTAT1,P-STAT1,STAT3,P-STAT3,PDL-1andβ-actin.ThecombinationtreatmentofvirusandRuxolitinibshowspromiseasaNSCLCtreatment.

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Presenter: QierraBrockmanPosterNumber: 11HomeInstitution: CoeCollegeProgram: LSSURPFacultyMentor: Dr.MichaelOlinResearchAdvisor: ElisabetAmpudiaMesiasPosterTitle: IdentificationoftheCD200ActivationReceptorSignalingPathwayAbstract: Glioblastomamultiformeisanincurableprimarybraintumor.Thestandardofcare

consistsofresectionfollowedbyradiationandchemotherapy,andisassociatedwithamedianoverallsurvivalof14.6months.Toaddressthisdismaloutcome,theFDAapprovedimmunecheckpointinhibitortherapyforsolidtumorsthatareotherwiserefractorytostandardtherapyheraldinganeweraforeffectivelytreatingcancer.Manyimmunecheckpointinhibitorsyieldpoorresponsesforpatientswithglioblastoma,callingintoquestionwhethercancerimmunotherapycanbeappliedtoglioblastoma.Wearetargetinganalternativecheckpointblockade(CD200blockade).TheCD200checkpointblockadeisapairedreceptorcomplexofinhibitoryandactivationreceptors.Targetingthesereceptorsactivateantigenpresentingcellsenhancingdendriticcellmaturation,cytokineproductionandantigenspecificTcellactivation,whichsignificantlyextendsurvivalintwomurinegliomamodels.AlthoughtheCD200checkpointisthemoststudiedofallimmunecheckpoints,thesignalingpathwaysurmountingtheinhibitorysignalsremainsunknown.ThisstudyisdesignedtodeterminethesignalingpathwayoftheCD200activationreceptor.Usingtranscriptionanalysis,wedeterminedpulsingmurineCD11bcellswithapeptidedesignedtoactivatetheactivationreceptorelicitedthetranscriptfoldincreaseofmoleculesassociatedwithimmuneactivation.

Presenter: CarolineBuchholzPosterNumber: 12HomeInstitution: IowaStateUniversityProgram: LSSURPFacultyMentor: Dr.NicholasLevinsonPosterTitle: BuildinganAuroraAKinaseFörsterResonanceEnergyTransfer(FRET)

BiosensorforInvestigatingConformationalPreferencesofKinaseInhibitorsAbstract: DisruptionofallostericregulationmechanismsinthekinaseAuroraA(AurA)is

linkedtomultipletypesofcancer.Thisproject’smainfocuswastobuildanAurAFRETbiosensorinordertoinvestigatetheconformationalpreferencesofpotentialinhibitors.Toconstructthebiosensor,AurAwaslabeledwithtwofluorophores,thedonordye(Alexa488)andtheacceptordye(Alexa568).Wethenusedanadvancedhigh-throughputTime-resolved(TR-)FRETplatform,whichisconcentrationindependent,tomeasuretheeffectsofsixknownkinaseinhibitorsonAurA.First,anewFRETpair(K227C-S284C)wascomparedtoapreviouslytestedpair(L225C-S284C).Thedatashowedthesameconformationalpreferences,demonstratingtherobustnessoftheresults.Thenextgoalwastoresolvedonoronlyeffectsobservedwiththepreviouslyuseddonorsite(L225C),duetoproximitytotheinhibitorbindingsite.WemeasuredtheD350Csiteandfoundithadlittletonoquenching,andsoisasuperiordonorsite.Thenextstepwouldbetodevelopawaytositespecificallyplacethedonordyeusingnonsensesuppressionandclickchemistry.Inthefuture,whenthebiosensorisbuilt,ahigh-throughputscreenofinhibitorscanbeperformedwithoutconfoundingeffectsofdirectquenchingfrominhibitors.

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Presenter: KarinaBurschPosterNumber: 13HomeInstitution: CatholicUniversityofAmericaProgram: LSSURPFacultyMentor: Dr.GregoryVercellottiPosterTitle: ACharacterizationoftheHemeBindingSiteonMD-2/TLR4Abstract: Insicklecelldisease(SCD),freehemereleasedbychronichemolysisbindsto

MD-2/TLR4andactivatesinflammatorysignalingcascadesthatproducemanycomponentsofSCDpathophysiology.LPS,thecanonicalTLR4ligand,bindstoMD-2/TLR4atasiteseparatefromthatofhemetoinitiatethesameinflammatorypathways.ThislabisworkingtocharacterizetheuniquehemebindingsiteonMD-2/TLR4inordertomitigateheme-inducedinflammation,whilepreservingtheinnateimmuneresponsetoLPS.BasedontheHemeBindalgorithm,site-directedmutagenesisofMD-2andNF-кBreporterassayshaveindicatedthatMD-2mutantsW23AandY34Asignificantlyinhibitheme-inducedNF-кBactivationinHEK293cells,butvariablyaffectLPS-inducedNF-кBactivation.ThecellularconcentrationofIL-8,achemokinewhosepromotercontainsanNF-кBbindingsitenecessaryfortranscription/translation,wasexaminedinanattempttoconfirmtheresultsofthereporterassays.HEK293cellsweretransfectedwithaplasmidcocktailcontainingTLR4,wtMD-2,CD14,andNF-кBreporterstomeasureIL-8productioninresponsetoLPS,TNF,and/orheminstimulation.ThecellularconcentrationofIL-8wasdeterminedbyELISAandqRT-PCRafterlysis.AlthoughinitialresultsdemonstratethathemeandLPS/heme-mediatedMD-2/TLR4signalingproducesmoreIL-8inHEK293cellsthanLPSalone,thisdifferenceisnotsignificant,duetolowtransfectionefficienciesinthecells.Therefore,theconcentrationofanothercytokineoranalternativemethodmayneedtobeusedtoconfirmtheresultsofthepastNF-kBreporterassaysinthisworkingmodel.

Presenter: PeterChristensonPosterNumber: 14HomeInstitution: BethelCollegeProgram: LSSURPFacultyMentor: CarrieWilmotPosterTitle: ProteinPathwaysfortheSynthesisofβ-LactonesAbstract: Betalactonemoleculesarepromisingantibioticsandanti-obesitydrugs.Allbeta

lactonescontainaconstrained,reactivefourmemberedring.Inrecentpublications,ourgrouphasshownthefirstpathwayforthecreationofbetalactonesusingOleproteins.Oleenzymesformlarge2.0MDacomplexesmakingCryo-EManidealtechniquetogainstructuralinsight.ByusingHis-tagpurificationmethodsandsizeexclusioncolumns,progresshasbeenmadetowardpurifyinghomogeneouscomplexes.HomogeneityiscriticalforCryo-EM.Inadditiontoprogressonstructures,ourgrouphassuccessfullypurifiedandistestinganotherproteincurrentlyknownasOrf1.ThisenzymeissuspectedoftoplayakeyroleinthecreationofebelactoneA.

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Presenter: DaphneCobbsPosterNumber: 15HomeInstitution: NorfolkStateUniversityProgram: LSSURPFacultyMentor: Dr.MatthewClarkPosterTitle: OptimizationofSRAPMarkersforMappingofVariegationinGrapevinesAbstract: Thepurposeofthisresearchistoidentifythemolecularmarkerslinkedtothe

trait,thatis,variegation.Oneissuethathasbeenobservedingrapebreedingisthewidespreadpresenceofvariegatedseedlings.Variegationistheappearanceofdifferentcoloredzonesintheleaves,andsometimesthestems,ofplants.Variegationisnotadesiredtraitbecausetheplantsthathavethisarelessefficientatphotosynthesisandoftensufferfromotherdiseases,whichmakethemcandidatesforcullingatthegreenhousestage.Thisrecessivetraitisinheritedfromtheparentsandoccursinabout25%ofseedlings.ThegeneticmarkersthatwereusedinthisexperimentwereSequenceRelatedAmplifiedPolymorphism(SRAP)markers.Thesemarkerswerechosenbecausetheyareaffordableandtheyareaneffectivewaytoidentifydominantmarkerslinked.Therewere176individualstestedfromthepopulationGE1642,whichwasderivedfromanMN1220xMN1326cross.TheGE1642populationwaspollinatedin2016andgrowninthegreenhouse.Theanticipatedgoalofthisstudyistodevelopamethodologyforthismarkersystemandfindnotabledifferencesinthegenomeoftheseedlingsinordertofindoutexactlywhatgene/alleleisresponsibleforvariegationinthegrapeseedlings.

Presenter: CamilaColón-AlfonzoPosterNumber: 16HomeInstitution: UniversityofPuertoRico-AreciboProgram: LSSURPFacultyMentor: Dr.Li-NaWeiResearchAdvisor: SungWookParkPosterTitle: RetinoicAcidAndCompound4BoundCellularRetinoicAcidBindingProtein1

RegulatesCaMKIIActivationAbstract: Calcium-calmodulinproteinkinaseII(CaMKII)isoneofthekeyenzymesforthe

regulationofnormalheartphysiology.Itisinvolvedinvariousheartdiseasessuchasischemiccardiaccelldeathandheartfailure.Ourlabhaspreviouslyfoundthatcellularretinoicacidbindingprotein1(Crabp1)modulatesCaMKIIactivation.HerewepresentevidencethatthisregulationmayoccurbydirectinteractionbetweenCrabp1andCaMKIIinthekinaseandregulatorydomain.Retinoicacid(RA)candampenCaMKIIphosphorylationthroughCrabp1andfurtherphospholamban(PLN)phosphorylationatThreonine17(T17),aCaMKIIsubstrate,inH9C2ratneonatalcardiomyocytes.Furthermore,compoundscreeningforpossibleCrabp1ligandsshowsthatcompound4(C4)reducesphosphorylationofCaMKIIandPLNatT17inducedbyouabain.InvitrocompetitionassaysuggeststhatRAandC4dampenCaMKIIactivationviaCrabp1bindingtoCaMKIIandcompetingoutcalmodulinfromthisenzyme.TheseresultssuggestthatRAandC4mayprotectheartfrompathologicalremodelingbysuppressingCaMKIIactivationthroughCrabp1.

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Presenter: SoniyaCoutinhoPosterNumber: 17HomeInstitution: MacalesterCollegeProgram: LSSURPFacultyMentor: Dr.AnnaLeePosterTitle: TheInvolvementofProteinKinaseCEpsilon(PKCε)inModulationofNicotine

AddictionAbstract: Alcoholandnicotineaddictionarehighlyprevalentandoftenco-morbid.Therearecurrentlyno

pharmaceuticalagentsthatcantreatbothaddictionssimultaneously.ProteinkinaseCepsilon(PKCε)isakinaseinvolvedinbothalcoholandnicotineaddictionmechanisms.PreviousstudiesshowthatmalePKCεknockout(PKCε-/-)micehavedecreasedalcoholconsumptionandreward,andmalePKCε-/-miceshowdecreasednicotineconsumptioncomparedtowild-typemales.IfPKCεalsoinfluencesalcoholandnicotineconsumptioninfemales,itcouldbeapotentialtargetforadrugtotreatco-morbidalcoholandnicotineaddiction.WeexaminedwhetherfemalePKCε-/-miceshowsimilarnicotineconsumptionpatternstomalePKCε-/-mice.FemalePKCε-/-andwild-typemiceweregiven4weeksofcontinuousaccessto15μg/mLnicotinewith2%saccharinsolutionandwaterwith2%saccharinsolutioninavoluntaryconsumptiontwo-bottlechoicemodel.Consumptionofnicotineandwaterweremeasured.Preliminarydata(n=5pergroup)showsnosignificantdifferenceinnicotineconsumptionbetweenwild-typeandknockoutmice(P=0.81).Ifourfindingremainsthesameinfuturestudieswithlargersamplesizes,thiswouldsuggestasexdifferenceinPKCεmodulationofnicotineconsumptioninmice.Specifically,PKCεinfluencesnicotineconsumptioninmalesbutnotfemales.Ifso,futureresearchshouldinvestigatemechanismsunderlyingthisdifference.Sexdifferencesarealsoobservedinhumansubstanceabuse,buttheirmolecularcausesarestillnotfullyknown.Thus,ourexperimenthasimportantimplicationsfortheroleofsex-influencedfactorsinaddictionmechanisms.

Presenter: ShelbyDavisPosterNumber: 18HomeInstitution: TennesseeStateUniversityProgram: LSSURPFacultyMentor: Dr.RobertMeiselPosterTitle: ExploringNovelBrainRegionsInFemaleSexBehaviorAbstract: Differentbrainregionsareconnectedanatomicallyandfunctionallyinvolvedinvarioussocial

behaviors.Ourlabisinterestedindeterminingwhichbrainregionsarespecificallyactivatedbysexualbehavior.Weknowthatthereareseparatecircuitsregulatingtheexpressionortherewarding/pleasurableconsequencesofsexbehavior.Ourlabhaspreviouslydemonstratedthatsexualbehaviorincreasesactivityinthenucleusaccumbens(NAc)andthemedialprefrontalcortex(mPFC),areastraditionallyinvolvedinsexualreward,butwewanttofurtherelucidateotherkeyregionsactivatedinthisevolutionarilyimportantbehavior.Wedidabroadscreenofthebrainandselectedfourbrainregionsimplicatedinrewardortheexpressionofsocialbehaviors.Fourfemalehamstersweregivenhormoneprimingfollowedbytenminutesofsexualexperience,andfourwereusedascontrols.Perfusionsfollowedanhourafterthesexexperience,atimeperiodthatwouldproducemaximalexpressionofc-Fos,whichisourmarkerofcellularactivity.Theirbrainswereslicedandunderwentimmunohistochemistrytostainforc-Fosactivationsothatwecouldimage,countandanalyzecellsinthedifferentbrainregions.Ourpreliminaryresultssuggestthatoutofallthebrainregionsstudiedwefoundtheinterpeduncularnucleus,lateralhabenula,superiorcolliculusandtheparaventricularthalamuswereactivatedduringsex.Inthisstudywehaveidentifiednovelbrainregionsthatwereactivatedduringfemalesexexperienceinhamsters.Followingexperimentswouldbedonetofigureoutwhatfunctionalcomponentsofsexbehaviorarerelatedtoeachofthesebrainregionswestudied.Furtherexperimentscancontroltheenvironmentandselectivelyinhibitregionsofinteresttoinformusoftheirfunctionalroleinsexualbehavior.

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Presenter: AngelDixonPosterNumber: 19HomeInstitution: XavierUniversityofLouisianaProgram: LSSURPFacultyMentor: Dr.MarkMasinoPosterTitle: TestingtheLocalizationofVariousDopamineReceptorswithintheZebrafish

NervousSystemAbstract: Dopamineisoneofthemanymodulatoryneurotransmittersstudiedduetoits

implicationinseveralneuralfunctionswhichinclude:neuroendocrineregulation,locomotion,motivationalbehaviors,learningandmemory.Wehavechosentofocusononeofitsfunctions,locomotion.Inzebrafish,dopamineisreleasedintothenervoussystembyasubsetofdopaminergicneuronswithinthebrain.Sincetherearefourdistinctdopaminereceptorswithinzebrafish,itisimportanttounderstandwhichdopaminereceptorsareexpressedinlocomotorcelltypes.Thus,leadingtothequestion,whatcelltypesrespondtothesignalssentfromdopaminergiccellbodieswithinthebrainandarethesecellsapartofeitherthespinalneuronsthatcontrollocomotionordopaminergicneuronswithinzebrafish?Usingimmunohistochemistryinlarvalzebrafish,wetestedantibodiesagainstdopaminereceptors1-4withinthespinalcordandbrain.Theresultsfromtheseindividualexperimentshavedeterminedthatthedopamine-2antibodyhasexpressedthemostsignalingwithinthediencephaloninbothglutamatergicanddopaminergictransgeniclinesofzebrafish.Inconclusion,dopaminereceptors1,3,and4haveillustratedminimalexpressioninboththespinalcordandbrainincomparisontothehighlevelofexpressionillustratedbythedopamine2receptor.

Presenter: GiovannaDorvelusPosterNumber: 20HomeInstitution: HowardUniversityProgram: LSSURPFacultyMentor: Dr.AlfonsoAraquePosterTitle: HippocampalAstrocyteResponsivenessToGlucocorticoidsAbstract: Stressisaphysiologicalanimalresponsetochallengingstimulifromtheenvironment.

Chronicandacutestressmayleadtopathologicaldisorderssuchasanxiety,depression,andpost-traumaticstressdisorder(PTSD).Glucocorticoids,atypeofcorticosteroidandsteroidhormonereleasedintheadrenalcortex,arekeysignalingmoleculesinvolvedinthestressresponse.Whilemechanismsofactionofglucocorticoidshavebeenwidelyfocusedonneuronsinvariousbrainregions,whetherastrocytessenseandrespondtothesestresshormonesislargelyunknown.Sinceastrocytesareemergingaskeycellularelementsactivelyinvolvedintheregulationofthesynapticfunctionintripartitesynapse,weaimedtoinvestigatewhethertheyrespondtoglucocorticoids,asaninitialapproachtotestthehypothesisthatastrocytescontributetotheeffectsofstressinthebrain.Usingcalciumimagingtechniques,fluorescentdyesandconfocalmicroscopyinmousehippocampalslices,wemonitoredtheintracellularcalciumlevelsofhippocampalastrocyteslocatedinthestratumradiatumoftheCA1region.Wequantifiedtheastrocyteactivitybeforeandafterapplicationofpregnenolone(XXµM).Ourpreliminaryresultsindicatethatpregnenoloneincreasesthecalcium-basedactivityofhippocampalastrocytes.Furtherstudieswilltestwhethertheseeffectsmayinfluencesynaptictransmission.Ifthatisthecase,astrocyteswouldplayanactiveroleinthepathophysiologyofstress,andwouldbeidentifiedasnovelcellulartargetsforthetreatmentofstress-relatedpathologies.

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Presenter: MorganEvensonPosterNumber: 21HomeInstitution: GustavusAdolphusCollegeProgram: LSSURPFacultyMentor: Dr.MartinaBazzaroPosterTitle: UNC-45AexpressionchangesduringdevelopmentofthenervoussystemAbstract: UNC-45AisamemberoftheevolutionarilyconservedUCS(UNC-

45/Cro1/She4p)proteinfamilythathasbeenassociatedwithmanyregulatoryfunctions.VariousstudieshaveimplicatedUNC-45Ainnon-musclemyosinII(NMII)-mediatedfunctionsincludingcytokinesis,cancercellproliferationandmotility,adhesion,andvesselformation.OurlabhasrecentlyshownthatUNC-45AisnecessaryforneuronaldifferentiationandelongationbyregulatingphosphorylationofNMII.GiventhenecessityforUNC-45Ainneuronalcytoskeletalfunctions,wesoughttoinvestigatehowUNC-45Aexpressionlevelsandlocalizationchangeduringdevelopmentusingimmunohistochemistry(IHC)andstainingtechniquesinmiceembryosandpost-natalday1(PND1)mousebrains.WefoundthatUNC-45Aiswidelyexpressedincorticalregions,eye,vibrissaefollicles,andskininembryos.ThisiscontrastingtoPND1astheexpressionisfoundprimarilyalongthedorsalpallium.Thus,weconcludethatUNC-45Aexpressiondeclinesthroughoutmammalianneuraldevelopment.FurtherworkisneededtoestablishhowlocalizationofUNC-45Achangesinthebodybeyondtheembryonicstage.

Presenter: JazzFieldsPosterNumber: 22HomeInstitution: TennesseeStateUniversityProgram: LSSURPFacultyMentor: Dr.RobertMeiselPosterTitle: ProbingtheRoleoftheMedialPrefrontalCortexinFemaleSexBehaviorAbstract: Itistypicallythoughtthatanimalsengageinsexprimarilyformeansof

reproduction.However,allanimals,includinghumans,actuallyperformthismotivatedbehaviorforitsrewardingconsequences.Indeed,studiesinourlabhavedemonstratedincreasedactivityfromsexinthenucleusaccumbens(NAc),akeyregionofrewardcircuity,aswellasinthemedialprefrontalcortex(mPFC),anareaknownforitsinvolvementingoal-directedbehavior.BecausethemPFCprovidesglutamatergicafferentstotheNAc,ourlabwantedtodetermineifactivationthatisseeninmPFCandNAcarerelatedinthesamecircuitry,actingindependently,orworkingtogetherasanintegratedunit.Todothisweexaminedtheexpressionofc-Fosininhibitory(GABA)andexcitatory(glutamate)neuronsinthemPFCtoelucidatewhichcelltypeisactivatedduringsextodeterminewhetherthemPFCisdrivingtheNAcactivity.ThemPFCneuronswerelabeledforbothc-Fos,amarkerofactivation,aswellasmarkersforGABA(GAD)orglutamate(CAMKII).Preliminaryresultssuggeststhatsexactivatesc-FosprimarilyintheCaMKIIneuronsofthemPFC.TheseresultsimplicatethemPFCandNAcasintegratedstructuresinrewardcircuitryinfemalesexbehavior.Futurestudiesmayhelprefinetherapeutictreatmentinsexualdesiredisordersinwomen,whichisaprevalentconcernaffecting10%ofthepopulation.Understandingsexandrewardcircuitryiscriticalindevelopingtherapiesforpathologicalconditionsandfurtherunderstandingsexualpleasureinbothmenandwomen.

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Presenter: RoshanakGonzalezPosterNumber: 23HomeInstitution: FloridaGulfCoastUniversityProgram: LSSURPFacultyMentor: Dr.GregMolnarPosterTitle: AnalyzingSleepinParkinson’sdiseasePatientsUndergoingDeepBrain

StimulationAbstract: Over1millionpeopleintheU.S.haveParkinson’sdisease(PD),mostwhomhavean

additionalaccompanyingsleepdisorder.OneofthemostpromisingtreatmentsforPDisdeepbrainstimulation(DBS)-implantedelectricallystimulatingleadsinthesubthalamicnucleusandglobuspallidusthatdecreasemotorsymptoms-mostnotablytremors.DespiteDBS’success,theissueofsleepdisordersinPDpatientsisunaddressed.Traditionalmethodsofanalyzingsleepincludepolysomnographyusingscalp-placedelectroencephography(EEG)electrodesandanalyzingrecordingsinreferencetoestablishedsleep-stageprofiles.ThegoalofthisstudyistocomparethesleepactivitysignalsfromEEGpolysomnographysignalstosubcorticallocalfieldpotential(LFP)recordingsfromanimplantedDBSlead.Thiswasdonebyusingscalp-placedEEGandDBSleadstotakebothcorticalandsubcorticalreadingsinapreclinicalmodelofPDandtoanalyzetheneuraloscillationsofsleep.EEGandLFPdataweretransmittedwirelesslytoaMatlabcomputerinterfaceusingTrianglesBiosystemsInternationalSystem(TBSI).Wehypothesizethatclassicsleep-stagerecordingwillbesimilarfromtheEEGandLFPsites.ModernDBSsystemsoffertheabilitytorecordLFPsthus,couldoffercliniciansmoreregularinsightintohowsleepdisturbancesmightbeaffectedbytheircurrenttreatmentregimen.

Presenter: IsabelleGonzalez-MontalvoPosterNumber: 24HomeInstitution: UniversityofPuertoRico-RioPiedresProgram: LSSURPFacultyMentor: Dr.DonaldSimoneResearchAdvisor: IrynaKhasabovaPosterTitle: ContributionOfExosomesIsolatedFromTheSciaticNerveOfCisplatin-

TreatedMiceToCisplatin-InducedHyperalgesiaAbstract: Cisplatinisacommonlyusedchemotherapeuticagentthattreatstumors.However,

theusageofthedrugislimitedbythedevelopmentofdose-dependentpainfulperipheralneuropathy.Ithasbeenshownthatbothdorsalrootganglion(DRG)neuronsandSchwanncellsareaffectedbycisplatin.Schwanncellsplayanessentialroleinmaintenanceofneuronalhealth.Exosomes,intraluminalvesiclesthatcontainmRNA,miRNA,proteins,andlipids,areapossiblemechanismofSchwanncell-DRGneuroncommunication.Theaimofthepresentinvestigationistodetermineifexosomesisolatedfromthesciaticnerveofcisplatin-treatedmicecontributetocisplatin-evokedhyperalgesia.Behavioraltestswereconductedtoevaluatetheeffectofexosomesonmechanicalhyperalgesiaandcoldsensitivity.Ourresultsdemonstratethedevelopmentofcisplatin-inducedmechanicalhyperalgesiaafterthefourthinjection.Exosomesisolatedfromthesciaticnervesofcisplatin-treatedmiceevokedhyperalgesiaafterthesecondinjection.Incontrasttocisplatin,noincreasedcoldsensitivitywasdeterminedinmicetreatedwithexosomes.Takentogether,ourresultssupportthecontributionofSchwanncell-derivedexosomestomechanicalhyperalgesia.

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Presenter: KathrynHagenPosterNumber: 25HomeInstitution: GustavusAdolphusCollegeProgram: LSSURPFacultyMentor: Dr.GeoffreyGhoseResearchAdvisor: ElisabethMoorePosterTitle: NeuralChangesinEarlyVisualAreasduetoPerceptualLearningAbstract: Visualperceptuallearning(VPL)istheabilitytoimprovetheperceptionofavisual

stimulusovertime.Lineorientationsandshapesareencodedintheearliestvisualregions,startingatV1andprogressingthroughV4,beforethemorecomplicatedregionsthatencodeentireobjects.StudyofearlyprocessingVPLisnecessarytounderstandmorecomplexregions.Inthisstudy,humansubjectsaretrainedonalearningtaskthatteststheirabilitytodistinguishacirclefromanoisybackground.Priortoandaftertrainingonthislearningtask,subjectsperformasecondmagnettaskduringfMRIscanning.Inthemagnet,subjectsdiscernaglitchwithindynamicallymorphingshapes.Wehypothesizethatbehavioralperformanceondetectingtheglitchincircleswillbecomparabletoother,non-circularshapespriortotrainingonthelearningtask.Followingtraining,performanceisexpectedtoimproveforthecircle,butnotforothershapes.InthefMRIsignal,voxelsthatareresponsivetoshapesinearlyvisualprocessingareasareexpectedtoshowalteredactivitywhenthecircleappears,comparedtovoxelsresponsivetonon-circularshapes,followingtraining.Thiswillprovidevaluablephysiologicalknowledgeconcerninghowneuralpopulationsprocessinformationtoreflectvisualperceptuallearning.

Presenter: SyedAliHassanPosterNumber: 26HomeInstitution: CUNY-HowardCollegeProgram: LSSURPFacultyMentor: Dr.ZhiYangResearchAdvisor: WenfengZhaoPosterTitle: BandwidthPursuit:ComparativeAnalysisofBinarySensingMatricesin

QuantizedCompressedSensingforNeuralSpikeDataCompressionAbstract: Wirelesstransmissionofneuralspikedatainrealtimeispowerconsuming.

Implantedstimulatorsandsensorshaveanupperlimitonsizeandpowerconsumptionplacedbybiologicalconstraints.Itisthereforerequiredtolowertheamountofdatatobewirelesslytransmitted.Quantized-Compressivesensingisonesuchmethodthatlowerstheamountofdatatobetransferredbyprojectingthequantizedsignalsintoalowerdimensionalspace.Thisdatacanthenberecoveredoff-chip.Theperformanceofquantizedcompressivesensingdependsonthesensingmatrixused,theratioofbitstomeasurementsinbandwidth,andtherecoveryalgorithmused.Traditionallyarandombinarymatrix(RBM)isusedasasensingmatrixbutiscomputationallyexpensive.Here,wecomparedtheperformanceof1-SparseRandomBinaryMatrix(1-SRBM)andQuasiCyclicArrayCodeMatrix(QCAC)vsRBM.Weperformedasweepofdifferentbitstomeasurementsratiosforfixedbandwidthstomaximizethesignaltonoiseratioforeachsensingmatrixused.ConsistentBasisPursuit(CoBP)recoveryalgorithmprovidedthebestresultsforallsensingmatrices.WeconcludedthattheperformanceofQCACandSRBMiscomparabletoRBMandthattheidealratioofbitstomeasurementsdependsonthesensingmatrixused.

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Presenter: AishwaryaIyerPosterNumber: 27HomeInstitution: UniversityofMD-BaltimoreCountyProgram: LSSURPFacultyMentor: Dr.ZoharSachsPosterTitle: IdentifyingGenesPertinentinTransformationfromMyelodysplastic

syndromestoAcuteMyeloidLeukemiainMurineModelsAbstract: Myelodysplasticsyndromes(MDS)areclonalmalignanciesthatare

characterizedbyineffectivehematopoiesis.Patientsoftenprogresstobonemarrowfailureorsecondaryacutemyeloidleukemia(sAML),whichtendstohavepoorprognosis.IdentifyingthegenesthatinstigatetransformationtosAMLwillaidinunderstandingthemechanismsthatdrivethisprocess.PreviousworkwasdonetodevelopatransgenicmousemodelthatestablishedMDSusingsleepingbeauty(SB)mutagenesisamongothermutations.SBmutagenesisisatechniqueusedtoknockoutgenesinmice.WeextractedRNAandDNAfrommiceharvestedtissuesafteroptimizingextractionprotocol.Afterassessingthequalityofnucleicacids,wewillthenperformligation-mediatedpolymerasechainreaction(LM-PCR)todeterminetheinsertionsitesofthesleepingbeautytransposon.UnderstandingthegeneticmakeupofthesemicewithSBmutagenesisinducedAMLwillallowforbetterunderstandingregardingtowhatgenesharborthepotentialforMDSpatientstodevelopsecondaryAML.

Presenter: AdrienneJoPosterNumber: 28HomeInstitution: ClaremotMcKennaCollegeProgram: LSSURPFacultyMentor: Dr.StanleyThayerResearchAdvisor: MatthewGreenPosterTitle: TheEffectsofHIV-1GP120ontheExpressionandPunctaCountofα5-

ContainingGABAAReceptorsinCulturedRatHippocampalNeuronsAbstract: Approximately50%ofthe>30millionpeopleworldwideaffectedbyhuman

immunodeficiencyvirus-1(HIV-1)sufferfromcognitiveimpairmentsknownasHIV-1-associatedneurocognitivedisorders(HAND).HIV-1caninfectmicroglia,leadingtothereleaseoftoxicproteins,suchasenvelopeglycoprotein120(gp120IIIB),whichcausesneurotoxicityandsynaptodendriticdamage.Gp120IIIBisknowntoinducethereleaseofinterleukin-1β(IL-1β),acytokinereleasedbymicroglia.PreviousworkshowsthatIL-1βincreasesthefunctionofα5-containingGABAAreceptors(α5-GABAA-Rs),whichlowerscellexcitabilityandmaycontributetocognitiveimpairments.Thus,wetestedwhethergp120IIIBwouldincreasetheexpressionofproteinclustersofα5-GABAA-Rsinprimaryhippocampalculturesderivedfromembryonicday17SpragueDawley®rats.Immunocytochemistrywasperformedtoexaminethelocalizationofα5-GABAA-Rsrelativetomicrotubule-associatedprotein2(MAP2)immunoreactivity.Basedonpreviouselectrophysiologyexperimentsonα5-GABAA-Rs,wehypothesizethatexpressionandpunctacountofα5-subunitproteinclusterswillincreaseafterexposuretogp120IIIB.Higherexpressionofα5-GABAA-Rsonneuronalmembranemightexplaintheincreasedneuronalinhibitionanddecreasedcellexcitabilityseeninvitro.AlteredexcitabilitymayleadtothecognitiveimpairmentsfoundinHANDpatients.Thus,inhibitionofα5-GABAA-RactivitymayserveasanoveltherapyforHANDpatients.

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Presenter: EunKimPosterNumber: 29HomeInstitution: DominicanUniversityProgram: LSSURPFacultyMentor: Dr.TimothyEbnerPosterTitle: CharacterizingInhibitoryInterneuronsandGliafromSCA8ModelsAbstract: SpinocerebellarAtaxiaType8(SCA8)isaneurodegenerativediseasecausedby

thetrinucleotide(CTG)repeatexpansionmutationoftheataxiageneATXN8.PhenotypesofSCA8includecerebellarandcorticalabnormalities.Recently,wehaveobservedincreasedcorticalexcitabilitytodirectelectricalstimulationinSCA8mice.Onepotentialmechanismforthisdysfunctioncouldbeduetothealterationsofinhibitoryinterneurons,eitherinstructureorfunction.ImmunohistochemistryisaprimemethodtowardsstudyingpotentialalterationininhibitoryinterneuronsinSCA8mousemodels.Tounderstandtheeffectsonthemotorcortexandcerebellum,welookedatinterneurons,microglia,andastrocytesbystainingforparvalbumin(PV),Iba1,andGFAP,respectively.Afterimagingtheimmunostainedtissuewithconfocalmicroscopes,thecelldensitiesofPV+andactivatedmicrogliaamongastrocyteswereobserved.AnalysisshowedthatthePV+celldensityprovedtobeinfavoroftheirregularexcitability.Thephenotypesofthegliainrelationtothediseasewerenotedaswell.Withtheseresults,theknowledgegainedfromthisprojectcouldhelpwiththeadvancementofnewtherapeuticstrategiesfortestingSCA8.

Presenter: AdamKornbergPosterNumber: 30HomeInstitution: UniversityofWisconsin-MadisonProgram: LSSURPFacultyMentor: Dr.JillSiegfriedResearchAdvisor: ChristianNjatcha,MariyaFarooquiPosterTitle: Short-TermEffectsofTargetingSTAT3inNSCLCUsinganOligonucleotide-

BasedDecoyAbstract: Thisstudyintendstoexploretheeffectsofanoligodeoxynucleotidedecoyto

selectivelyinhibittheactivatedphosphorylateddimeroftranscriptionfactorSTAT3inNon-SmallCellLungCancer(NSCLC)tumorsafterjustfivedaysinamousemodel.Ithaspreviouslybeenobservedthattreatmentwiththedecoyfor29daysinmicewithhumanNSCLCtumorcellxenograftsledtosignificantreductionintumorareaandextensivenecrosis.Toexploretheeventsthatprecededthenecrosisandtumorareareduction,theeffectofthedecoywasobservedafterfivedaysoftreatment.Itwashypothesizedthatafterfivedays,therewouldbeareductionintumorcellproliferationandanincreaseinapoptosisintumortissueduetotheinhibitionofpSTAT3.Usingimmunohistochemistry(IHC),variationsinproteinexpressionbetweenoligodeoxynucleotidedecoyandmutantcontroltreatmentswereimagedandanalyzedwithagradingscale.IHCanalysisoftheactivatedtranscriptionfactorpSTAT3andcellproliferationmarkerKi-67showeddecreasedstaininginthepresenceoftheoligodeoxynucleotidedecoy.TherewasnosignificantdifferenceinstainingintensitybetweendecoyandmutantcontroltreatmentsforapoptosismarkerCleavedCaspase-3.ThisallowsustoconcludethatcellularproliferationandactivatedSTAT3decreaseintumortissueafterjustfivedays,whileapoptosisisunaffected.

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Presenter: ThomasKrugPosterNumber: 31HomeInstitution: MinnesotaStateUniversity-MankatoProgram: LSSURPFacultyMentor: Dr.DanielSchmidtPosterTitle: ModelingNeuralNetworkinAidtoDevelopingOptogeneticReagentsAbstract: Controllingneuralactivitywithhighspecificityusingprinciplesof

optogenetics—highprecisionandgeneticallyencoded—iscrucialforunderstandinghowcellularcomponentscontributetoneuraldynamics.Weapplytheseprinciplesbyharnessingthediversityofpeptidetoxinstotargetspecificcellularcomponentssuchasionicconductancesandsynapticconnectionswithchemicalreagentscalledlumitoxins.Tobetterunderstandhowlumitoxinsaffectneuronalactivity,wemodelledaneuralnetworkofrathippocampalcellsinMATLABandcomparedtheeffectsofsodiumandpotassiumconductancesandsynapticconnectionstoneuronspikingfrequency.Oursimulationssuggestthatpotassiumchannelmanipulationcausessignificantchangesinspikefrequencyandoverallnetworkdynamicsindicatingtheutilityofpotassiumtargetedlumitoxins.Ournextstepistorecordandcompareexperimentallumitoxinresultstooursimulatedresults.

Presenter: EdeneShirleyLakpaPosterNumber: 32HomeInstitution: HowardUniversityProgram: LSSURPFacultyMentor: Dr.HarryOrrPosterTitle: CharacterizationofSpinocerebellarAtaxiaType1MouseModelPcp2

[82Q]W775RAbstract: SpinocerebellarAtaxiaTypeI(SCA1)isanautosomaldominant

neurodegenerativedisordercausedbytheexpansionofCAGrepeatsencodingapolyglutamine(polyQ)tractintheATXN1protein.PrimarilyaffectingPurkinjecellsofthecerebellum,pathologyinSCA1iscausedbytheenhancedinteractionbetweenATXN1andsplicingfactorRBM17,alteringexpressionofothergenes.PreviousexperimentsconductedbythelabdevelopedPcp2[82Q],amousemodelwithoverexpressionofthepolyQtractintheATXN1gene.Inthisstudy,Pcp2[82Q]W775R,atransgenicmousemodel,wasgenerated.Itisanoverexpressionmodelwithan82polyQtractintheATXN1proteinaswellasthereplacementoftryptophanwitharginineataminoacid775oftheATXN1gene.WeproposethissubstitutionthatdisruptstheabilityofATXN1tobindtoRBM17willresultinthedampeningofSCA1.TocharacterizeW775R,RNAexpressionwasdeterminedbyqPCR,proteindistributionandexpressionbyimmunofluorescenceandwesternblotting.ResultsindicatethattwoW775RlinesexpressthepolyQtractcomparabletothePcp2[82Q]mousemodel.RNAsequenceofthesemicewillbeusedtolookattheeffectsATXN1[82Q]W775RhasonRNAsplicing.Thismayelucidatepathwaysthatcanbeutilizedfordiseasetherapy.

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Presenter: PhilipLeungPosterNumber: 33HomeInstitution: UniversityofMinnesota-TwinCitiesProgram: LSSURPFacultyMentor: Dr.BurckhardSeeligPosterTitle: DiscoveryOfActivityImprovementsInARNALigaseMutantLibraryViaAHigh

ThroughputMalachiteGreenScreeningProtocolAbstract: Acommonapproachinthedisciplineofproteinengineeringistheapplicationof

directedevolution.Directedevolutionexperimentsareusedtoselectinvitroorinvivoforimprovedenzymaticfunction,resultinginverylargelibrariesofmutantswithpotentialimprovements.Therefore,thedemandforspecifichighthroughputscreeningprotocolstodetectimprovementsiscontinuouslyescalating,asthevarietyofproteinsundergoingengineeringexpands.Here,weshowaprotocolusedtodetectcatalyticrateincreasesinamutantlibraryderivedfromanovelRNAligaseenzyme.Theenzymecatalyzesareactionnotfoundinnature,wherebya5'triphosphorylatedRNAoligonucleotideiscovalentlylinkedinstandardbiologicalconfigurationtoanotherRNAoligonucleotideinthepresenceofacomplementaryDNAsplint,andreleasingpyrophosphateasaleavinggroup.Theassaydetectsphosphatelevelsinsolutionafterapyrophosphataseliberatesphosphatefromthefreepyrophosphate.Theprotocolhashighsensitivityandusescheap,easilyavailablereagents,andrequiresonlyequipment,whichisstandardtomostlaboratoriesequippedtoresearchmolecularbiology.Inaddition,theworkflowprocesscandifferentiatebetweenupto96uniquemutantsinasingleassay.Afinaladvantageoftheprotocolisthatitcanbeusedtodetectrateenhancementsinanyreactionwhichreleasesphosphateorpyrophosphate.TheassayrepeatedlydetectedRNAligasemutantswithhigheractivitieswithlowerror,demonstratingitsefficacyinnarrowingthepoolofenzymecandidateswithwhichtocontinueengineeringprojects.

Presenter: QuangLyPosterNumber: 34HomeInstitution: CaliforniaStateUniversity-LongBeachProgram: LSSURPFacultyMentor: Dr.BinHePosterTitle: ImplementationofFootMotorImaginationinBrain-ComputerInterfaceAbstract: Brain-computerinterfaces(BCI),basedondataextractedandanalyzedfrom

electroencephalographic(EEG)signalswhiledistinctmentaltasksareperformed,areeffectivetoolsinassistingpeoplewithseriousmotorimpairmentsrangingfrompartialparalysistofulllocked-insyndrome.ConventionalBCIfeedbacksystems,however,requireextensivetrainingtimesinorderforsubjectstoperformmotorimagerytasksproficiently.Inourexperimentalprotocol,eachsubjectcompletedanofflinetrainingandonlinefeedbacktest,inwhichsubjectsmovedacursoronthecomputermonitorwiththeonlyinputbeingbrainsignals.Offlinetrainingdeterminedtheuser-specificfrequencybandthatcorrespondedtofootmotorimagination.Duringtheonlinesessionsrawneurologicaldatawasprocessedinrealtimetocorrelateto4outof5mentalstates:lefthandimagery,righthandimagery,imaginingbothhands,andeitherfootimageryortherestcondition.Preliminaryresultssuggestanimprovementwhenincorporatingfootmotorimaginationrelativetoarestingtask.Futureiterationsofthisexperimentalprotocolwillinvolvevirtualreality(VR)topotentiallyreducethetrainingtime.ItisourhypothesisthattheinclusionoffootmotorimagerywillresultinagreaterdegreeofcontrolforBCItasks.

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Presenter: AllenLynchPosterNumber: 35HomeInstitution: UniversityofMinnesota-TwinCitiesProgram: LSSURPFacultyMentor: Dr.JeffreyGralnickPosterTitle: TheBetterTwin:FindingtheComponentofShewanellaOneidensisUshAthat

PromotesFlavinSynthesisAbstract: Shewanellaoneidensisisametabolically-diversemarinebacteriumthatpossessestheabilityto

respireusingaremotefinalelectronacceptorinanoxicconditions.Inconditionsnecessitatingtheuseofthisextracellularelectrontransport,Shewanellaprimarilyutilizesthemoleculeflavinmononucleotide(FMN)asashuttletocarryelectronsandreducemoleculesintheenvironment.ElectronexporterFMNissynthesizedbycleavageofflavindinucleotide(FAD)bytheperiplasmicproteinushA.Additionally,ShewanellaUshAperformsthedephosphorylationofadenosinemonophosphate(AMP).E.colialsoproducesanushAproteinthatshares50.5%aminoacididentitywiththeShewanellaproteinthatalsocleavesAMP,however,theE.colienzymeisvastlylessreactivewithFAD.ThispaperexploresthedifferencesbetweentheShewanellaandE.coliUshAvariantsthat,despitehavingagreatdegreeofaminoacidcommonality,havestarklydifferentcatalyticefficienciesregardingFADcleavage.ThefirstapproachtodeterminingthedifferenceswasamplifyingexpressionofShewanellaUshAusingaplasmidcontainingapromoterforT7high-efficiencyRNApolymerase.Increasedexpressionwasutilizedforpurification,followedbyanalysisusingcyro-electronmicroscopy.AsecondapproachinvolvedconstructingaplasmidcontainingtheShewanellaushAgenewithselectaminoacidsintheactivesitechangedtoresembletheactivesiteofE.coliUshA.ThiseditedUshAallelewastransformedintoShewanella,thenitscatalyticactivitywithrespecttoFADwasobservedusinganFADcleavageassay.

Presenter: ElizabethMacDonaldPosterNumber: 36HomeInstitution: UniversityofMinnesota-TwinCitiesProgram: LSSURPFacultyMentor: Dr.CaraSantelliPosterTitle: IdentificationofCultivableSeleniumTolerantMicroorganismsIsolatedfrom

SeleniumContaminatedMineSoilAbstract: Seleniumpollutionisaglobalenvironmentalproblemimpactingbothhumanandenvironmental

health.Seleniumisanessentialnutrientbuthasasmallmarginbetweendeficiencyandtoxicityandbiomagnifiesinthefoodchain.Microorganismsplayacrucialroleinredoxtransformationsofseleniumintheenvironment,whichinfluenceitssolubilityandbioavailability.Themoreoxidizedforms,Se(IV)andSe(VI),aresoluble,toxic,andbioavailable.MicroorganismscanreducethesetoSe(0)andSe(-II),whichareinsolubleandlesstoxic.ThoughtheyareessentialformanyenvironmentalSetransformations,currentunderstandingoforganismsarecapableoftoleratingandtransformingSeislimited.Identifyingorganismsthatarecapableoflivinginhigh-seleniumenvironmentsandperformingthesetransformationsisimportantforunderstandingseleniumcyclingandidentifyingorganismsthatcouldbeusedinbioremediation.Bacteriaandfungiwereisolatedfromselenium-contaminatedsoilfromtworeclaimedphosphateminesinSoutheasternIdaho.Organismswereisolatedusingthreedifferentmediatypesamendedwitheither100uMSe(IV)[asNa2SeO3]orSe(VI)[asNa2SeO4].Toidentifytheorganisms,the16SribosomalRNA(rRNA)generegionfrombacteriaandtheinternaltranscribedspacer(ITS)rRNAgeneregionfromfungiwereamplifiedandsequencedusingSangerSequencing.IsolateDNAsequenceswerealignedusingBenchlingthenputintophylogenetictreesusingArbtodeterminethemostcloselyrelatedpreviouslycharacterizedspecies.TheorganismswerealsogrowninmediacontainingSe(IV)andSe(VI)todetermineiftheyareabletoreduceselenium.Outof80bacterialisolates,14uniquestrainshavebeenidentifiedandphylogeneticallycharacterized.ThemostabundantbacterialgenerainthesequencedisolateswereArthrobacterandPseudomonas,withfourspeciesidentifiedeach.

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Presenter: DelfinaManceboPosterNumber: 37HomeInstitution: ProvidenceCollegeProgram: LSSURPFacultyMentor: Dr.MarkThomasPosterTitle: CharacterizingPlasticityChangesInCorticostriatalEnsemblesAbstract: Thenucleusaccumbens(NAc)hasbeenshowntosignalrewardinformationand

undergomaladaptivechangesrelatedtoaddiction.Untilrecently,directlymeasuringchangesinstrengthofsynaptictransmissionbetweentheNAcanditsvariousupstreaminputscouldnotbefullydiscerned.Tostudythis,weintroducedchannelrhodopsin-2(ChR2,alight-sensitiveionchannel)tooneoftheNAcinputs,theinfralimbic(IL)sub-regionoftheprefrontalcortex,inC57bl6jmice.TheChR2genewasdrivenbyacalcium-calmodulin-kinase-2promoterinanadeno-associatedviralconstruct(AAV8)totargetexpressiontopyramidalneuronsintheILcortex,whichareknowntosendexcitatoryprojectionstotheshell(Sh)oftheNAc.TointerrogatefunctionalconnectivityoftheIL-NAcShcircuit,localfieldpotentials(LFPs)oftheNAcShwererecordedinacuteexvivoslicepreparationsandevokedbyshiningabluelightdirectedatILafferents.Lightstimulationevokedanegative,bimodalwaveforminLFPs,consistentwithanILpre-synapticdepolarizationresponsefollowedbyasecondNAcShpost-synapticdepolarizationresponse,thelatterofwhichisbothcalcium-andglutamate-dependent.Wethendeliveredapatternofstimulationknowntoinduceaformoflong-termdepression(LTD,4mspulses-10hz-10min)andvalidatedthatwecouldreducetheamplitudeofthesecondpeakinIL-NAcShopto-evoked-LFPs.Lastly,wedevelopedanexvivoassaytocomparefunctionalconnectivitymeasuresbetweensubjectsbynormalizingpost-synapticresponsestoafferentrecruitmentsizeineffortstocaptureinvivoexperience-dependentplasticitychangesinspecificstriatalcircuitsmeasuredatthepopulationensemblelevel.

Presenter: AudreMayPosterNumber: 38HomeInstitution: LewisandClarkCollegeProgram: LSSURPFacultyMentor: Dr.SubreeSubramanianResearchAdvisor: XiandaZhaoPosterTitle: MicroRNA-552RegulatesAtypicalChemokineReceptor4AndChemokine

ReceptorCCR7-DependentDendriticCellChemotaxisInColorectalCancerAbstract: AntigenLoadingdendriticcells(DCs)arecriticalforaneffectiveadaptiveimmuneresponse,as

naiveTcellsareactivatedoncetheirTcellreceptorsrecognizeantigenspresentedbymajorhistocompatibilitycomplex(MHC)classIIpeptides.InorderforTcellactivationtooccur,DCsmigratefromtumortissuetotumordraininglymphnodes.DCchemotaxisisregulatedbyCC-chemokinereceptor7(CCR7)activation,whichisdrivenbyitsligands,chemokinesCCL19andCCL21.Howeverincolorectalcancer(CRC),expressionofthesechemokinesisdysregulated.Apotentialfactorcontributingtothisirregularityisatypicalchemokinereceptor4(ACKR4)expression.ACKR4sequestersCCL19andCCL21inperipheraltissue,helpingtomaintainthechemokinegradient.InCRCtumortissue,researchsuggestsACKR4expressionisdownregulated,whilemicroRNA-552expressionisupregulatedincolorectalcancertumortissue.HerewedemonstratelowexpressionofACKR4atbothtranscriptandproteinlevels.WealsoexplorethepotentialsilencingcapabilitiesofmicroRNA-552targetingACKR4expressioninCRCtumortissue.CorrelatingexpressionpatternssuggestthatmicroRNA552istargetingACKR4,furtherelucidatingmechanisticdisruptionstoCCR7-dependentdendriticcellchemotaxis.

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Presenter: SarahMeierPosterNumber: 39HomeInstitution: UniversityofNewHampshireProgram: LSSURPFacultyMentor: Dr.DavidRedishPosterTitle: InfralimbicVersusPrelimbicCorticesInDeliberativeLearningAndProcedural

LearningSystemsAbstract: Differingdecision-makingsystemscanbefoundinseveralregionsofthebrain.

Ofparticularinteresttothisprojectaretworegionsofthemedialprefrontalcortex:theprelimbicandinfralimbiccortices.Theprelimbicregionisbelievedtobeinvolvedinadeliberate-planningsystemwhichcanbeevidencedbythevicarioustrialanderrorphenomenon,whereastheinfralimbicregionisbelievedtobeinvolvedinahabit-formingsystem,evidencedbythepathstereotypyphenomenon.Conflictbetweentheseregionsariseswhenfacedwithasingledecision.Therefore,thegoalofthecurrentprojectwastodeterminehowthatconflictisresolved.ThiswasdonebyactivatingDREADDswithineithertheprelimbicorinfralimbicregionoftworatsandanalyzingforthesebehavioralphenomenawhenputthroughaContingencySwitchmazetask.Ifwefindanincreaseinpathstereotypywhentheprelimbicregionisdisrupted,oranincreaseinvicarioustrialanderrorwhentheinfralimbicregionisdisrupted,thiswouldimplythattheregionnotdisruptedgainscontroloverresultantbehaviorgivensystemconflict.

Presenter: BriannaMoralesPosterNumber: 40HomeInstitution: UniversityofTexas-SanAntonioProgram: LSSURPFacultyMentor: Dr.VictorBarocasPosterTitle: UnderstandingVibrotactileSensingOfSimpleAndComplexWaveformsAbstract: Psychophysicalexperimentswereconductedtocharacterizehumanresponseto

vibratorystimuliatvariousfrequencies.TheaimofthisstudywastounderstandthePaciniancorpuscle,atouchmechanoreceptorwithinthehandresponsiblefordetectinghighfrequencies.Weinvestigatedthediscriminabilityoffivedifferentfrequencies(160,230,310,400,and500Hz)anddeterminedwhetherplayinganunderlyingfrequencywouldimprovethesubjects’abilitytodifferentiatethestimuli.Inthefirststudy,subjectswerepresentedwith40pairsofconsecutivefrequencieswithinthereportedreceptiverangeofthePaciniancorpuscle(theconsecutivefrequenciesare160,230,310,400,and500Hz).Subjectswereaskedtodifferentiatebetweentwofrequenciesinsame-differenttests,respondingtoagraphicaluserinterfacedevelopedinMATLAB.Then,thestudywasrepeated,exceptthat100Hzoscillationwasappliedinconjunctionwitheachindividualfrequencytoproducecomplexwaveforms.Theparticipantswereabletodiscriminatebetweenthesimplewaveformfrequenciesmoreeasilyinthefirstexperimentcomparedtothesecondsetupwiththecomplexwaveform.Thenextstepinthisstudyistoanalyzethed'valuesforthesubjects,inordertodeterminetheirsensitivity.

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Presenter: DavisNossamanPosterNumber: 41HomeInstitution: HardingUniversityProgram: LSSURPFacultyMentor: Dr.MatthewJohnsonPosterTitle: AGloveDesignforQuantifiableRigidityTestinginParkinson’sDiseaseAbstract: CogwheelmusclerigidityisoneoftheprominentmotorsignsinParkinson’sdisease

patients.Toquantifyparkinsonianrigidity,awell-trainedmovementdisordersspecialistslowlyarticulatesapatient’sjointsandratestheperceivedlevelofresistancetothemovementonaninteger-basedscalefrom0(norigidity)to4(severerigidity)foreachjoint.Thesubjectivityofthismotorexamleadstointra-andinter-ratervarianceofrigidityscoringandlowscoringresolution,whichcombinetoyieldunreliableresultsregardingtheeffectivenessofapatient’streatmentregime.Toaddressthisclinicalchallenge,wedevelopedamulti-modalsensorglovethatintegratesaninertialmeasurementunitandtwoforcesensorsattachedtothethumbandindexfingers.SignalsdetectedfromthesethreesensorsweremeasuredthroughanArduinosystem.Theglovewasevaluatedusing(1)aphantomelbowjointwithvariableresistanceand(2)aparkinsonianresearchanimalbothoffandondeepbrainstimulationtherapy.Thedeviceislightweight,user-friendly,andcapableofexaminingrigidityacrossmultiplejoints,makingitareasonablecandidateforimplementationinaclinicalsetting.

Presenter: JaimePérezLizardiPosterNumber: 42HomeInstitution: UniversityofPuertoRico-RioPiedresProgram: LSSURPFacultyMentor: Dr.DavidA.PotterResearchAdvisor: ZhijunGuoPosterTitle: CytochromeP450RegulationofBreastCancerMitochondriaAbstract: Cytochrome P450 (CYP) enzymeswith arachidonic acid (AA) epoxygenase activity

promote breast tumors, in part, through epoxyeicosatrienoic acids (EETs)biosynthesis and are potential therapeutic targets. Immunocompetent mousemammarytumormodelsthataredependentonmurineCypAAepoxygenaseactivitymayadvanceourunderstandingofthisnovelpathway.However,itisunknownwhichmammary tumormodelsmay be dependent on CypAA epoxygenase activity andwhich murine Cyps are expressed in mouse breast tumor cells. To answer thesequestions,severalmousebreastcancercell linesweresurveyedforsensitivitytoahighlypotentchemicalprobeinhibitorofCypAAepoxygenaseactivity,hexyl-benzyl-biguanide(HBB).Wefoundthattherewere2estrogenreceptorpositive(ER+HER2-)cell linesSSM2ucdand67NR,aswellas2basalcell lines, (ER-HER2-),whichweresensitivetoHBBwithIC50valuesoflessthan25µM.WethenconductedasurveyofmouseCypenzymeswhicharecandidateAAepoxygenases.FirsttotalmRNAsoftherespectivecelllineswereextracted,thenusingRT-PCR,acDNAlibrarywascreated.DifferentCypgeneprimerswereusedtoprobethecDNAlibrary,todeterminewhichCypmRNA species are present.Westernblot analysiswill beused to confirm theprotein expression of the Cyps. Finally, using immunofluorescentmicroscopy, thelocalizationoftheseproteinswithinthecellwillbeassessed.ItisexpectedthatCypepoxygenase enzymeswill be localizedwithinmammary carcinomamitochondria,similartothelocalizationofCYP3A4inthehumanMCF-7breastcancercellline.

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Presenter: ElliottPetersonPosterNumber: 43HomeInstitution: PacificLutheranUniversityProgram: LSSURPFacultyMentor: Dr.DouglasYeePosterTitle: ExaminingtheEffectsofGp2ProteinScaffoldsonIGF1R/InsRSignalingin

Triple-NegativeBreastTumorCellLinesAbstract: ThetypeIinsulin-likegrowthfactorreceptor(IGF1R)andinsulinreceptor(InsR)

signalingpathwayinbreasttumorsiswellunderstood,andhasledtothedevelopmentofnumerousdrugstargetingthissystem.Unfortunately,clinicaltrialstestinganti-IGF1Rmonoclonalantibodieswerenotsuccessful.InsR,acloselyrelatedreceptortoIGF1Rhaspurposelybeenavoidedasapotentialcancertargetduetounwantedmetabolicsideeffects.SmallproteinscaffoldsbasedontheT7phagegene2protein(Gp2)havebeendevelopedtotargetInsRandhavebeenshowntobeeffectiveininhibitingendocrine-resistantbreastcancergrowth.However,theefficacyoftheseGp2intriple-negativebreastcancercellsisstillelusive.Here,weexaminetheinhibitoryeffectsofGp2inatriple-negative(MDA-MB-435)LCC6celllinebymeasuringthedownstreamactivationofAKT,whichisamajoroncoproteinincellproliferationandmalignantphenotype.LCC6cellswereplated,serum-starvedandtreatedindividuallywithGp2variants#1,#5,and#10overnight,andthenexposedtoeitherinsulin,IGF-I,orIGF-IIfor15minutes.ThesecellswerecollectedandlysedforWesternblotanalysis.PreliminaryanalysisoftheseblotsdemonstratedthatGp2#1fullyblockedinsulin-stimulated,butonlypartiallyinhibitedIGF-IandIGF-IIstimulatedAKTsignalinginLCC6cellscomparedtountreatedcells.Gp2#5and#10resultswerenotcompleteduetosometechnicalissues;however,weanticipateaninhibitoryeffectofGp2#5and#10ininsulinsignaling.Thus,InsRisaneffectivetargetfortreatingtriple-negativebreasttumors.

Presenter: StephaniePonce-RoblesPosterNumber: 44HomeInstitution: UniversityofPuertoRico-AguadillaProgram: LSSURPFacultyMentor: Dr.TanyaFreedmanPosterTitle: InflammationUpregulatesLynAExpressionandβ-glucanSensitivityin

MacrophagesAbstract: JuvenileIdiopathicArthritis(JIA)isanautoimmunediseaseinwhichmacrophagecellshelpto

drivechronicinflammation.Currentantirheumaticdrugsblockinflammatorymacrophages,butalsosuppressmacrophageimmunefunction.Large-scaleclusteringofimmunoreceptortyrosine-basedactivationmotif(ITAM)-coupledreceptorsinitiatesantimicrobialresponsesinmacrophages.Exposuretoinflammatorycytokines(e.g.IFN-γ)canlowerthethresholdformousemacrophageactivationbyupregulatingtheSrc-familykinaseLynA,causinghypersensitivesignaling.IFN-γiselevatedinJIApatients,whichmayinduceLynA-mediatedhypersensitivemacrophagesignaling.Therefore,inhibitingLynAsignalingmaybeanefficienttreatmenttotargetinflammatorymacrophagesinJIAwithoutsuppressingantimicrobialimmunity.Istimulatedmousebonemarrow-derivedmacrophages(BMDMs)withβ-glucanITAM-receptorligandstodetermineifLynAsignalingisrequiredformacrophagesensitivitytophysiological“weak”(non-clustering)stimuli.Ialsoculturedhumanmonocyte-derivedmacrophagesandstimulatedthemwithIFN-γtotestLynAupregulation.MyimmunoblotdatasupportedpreviousstudiesdemonstratingthatmacrophagedownstreamsignalingthroughDectin-1pathwayisaLyn-andpriming-dependentprocess.Ourlong-termgoalistoinhibittheLynApathwaytoblockhypersensitivemacrophagesignalinginJIApatientswithoutsuppressingtheimmunesystem.

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Presenter: SidharthRameshPosterNumber: 45HomeInstitution: UniversityofPennsylvaniaProgram: LSSURPFacultyMentor: Dr.TimothyStarrPosterTitle: SingleCellSequencingAsAPrognosticAndPredictiveToolForOvarianCancer

TherapyAbstract: Technologicaladvancesallowgenomicanalysestobeconductedatthesinglecelllevel.Analysisof

geneexpressionatthisdetailedlevelcouldleadtoprognosticandpredictivebiomarkersalongwithenhancedunderstandingofstromalandcancercellsubpopulationsincludingstemcellsandchemotherapyresistantpopulations.Thisprojectprospectivelystudiesthetranscriptomesofhighgradeserousovariancancersolidtumorsamplesatthesinglecelllevel.Wehaveenrolled8patientsandbegunsinglecellRNAsequencingthetranscriptomesusingthe10XGenomicsplatform.Thesepatientsarereceivingcarboplatin/paclitaxeltreatmentandwillbefollowedprospectively;theirclinicalresponseswillbeincorporatedintoouranalyses.Usingtheplatform,wehavecompletedRNAsequencingoffivepatients.Wequantifiedgeneexpressiononanaverageof8,707cells/patientand1,723genes/cell.Usinggraph-basedclusteringcombinedwiththet-DistributedStochasticNeighborEmbeddingtechniquefordimensionalityreduction,weidentifiedapproximately9to15subsetsofcellswithinthesecancersamplesbasedonanalysisoftheirgeneexpressionpatterns.UsingbioinformatictoolsincludingCellRanger,Seurat,andIngenuityPathwayAnalysis,wedefinedseveralsubsetsincludingimmunecells,stromalcellsandcancerepithelialcellsbasedonknownfunctionalmarkers.Wecanestimatethefrequencyofeachsubsetandsubdividethegroupsusingcell-typespecificmarkers.Ultimately,wewillcorrelatepresenceandpercentageofcellsubpopulationswithclinicaloutcomesofthepatients.Ourlong-termgoalistousesinglecelldataasaprognosticbiomarkerforchemotherapyresistanceaswellasatoolforpredictingeffectivetherapeuticoptions.

Presenter: EmilyReevesPosterNumber: 46HomeInstitution: OberlinCollegeProgram: LSSURPFacultyMentor: Dr.LucyVulchanovaResearchAdvisor: JenniferCook,ReshmaGore,MaureenRiedlPosterTitle: EffectsofPeripheralNerveInjuryonC3aR1ExpressionintheSpinalCordAbstract: Chronicpainisaproblemaffecting100millionadultsintheU.S.,andacutepainduetoinjurycan

transitionintoachronicstateafterneuroplasticityhastakenplaceinthespinalcord.VGFisaneuropeptideprecursorproteinthatisupregulatedfollowinginjury,andourlabhaspreviouslyfoundthatVGFisinvolvedinneuroplasticityassociatedwithchronicpain.ThemechanismofVGFcontributiontohypersensitivityafternerveinjuryislessunderstood.TheVGF-derivedpeptideTLQP-21hasbeenfoundbyourlabtocontributetothedevelopmentandmaintenanceofneuropathicpainfollowingperipheralnerveinjury,anditsreceptorC3aR1isacomplementreceptorassociatedwiththeinnateimmunesystem.WeaimedtoinvestigateC3aR1inthespinalcordinordertoprobehowitsexpressionchangesfollowingperipheralnerveinjury.WehypothesizedthatC3aR1expressionwouldincreaseafterinjuryandchangeovertime.Sparednerveinjury(SNI)wasperformed,andtissuewascollectedat3,14,and28dayspost-SNI.ThroughimmunohistochemistrytheC3aR1receptorwasstained,andexpressionwasmeasuredinthedorsalhornofthelumbarspinalcord.AllthreetimepointsshowedanincreaseofC3aR1expressionintheinjuredmicecomparedtotheshamcontrols.ThepeakincreaseofC3aR1expressionoccurredat14dayspost-SNI.TheseresultsindicatethattherewasanoverallincreaseinC3aR1signalingpost-injuryandthatthispeaksat14dayspost-SNI.FurtherstudieswillbefocusedonhowtheinvolvementofC3aR1signalingchangesovertimeafterinjury,inadditiontoprobingthemechanismofthereceptor’sinvolvementinhypersensitivityfollowingSNI.

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Presenter: IsabelRickePosterNumber: 47HomeInstitution: UniversityofMinnesota-TwinCitiesProgram: LSSURPFacultyMentor: Dr.SatoshiIshiiPosterTitle: ImpactofMigratoryBirdsonWaterQualityAbstract: GeeseareknowntoharbormanybacterialpathogenssuchasCampylobacter

andArcobacterthatarehazardoustohumanhealth.Asaquaticbirdsthatcongregateinlargenumbersandproducelargequantitiesoffecalmaterial,geeseareofgreatconcerntowatersafety.ThisstudysoughttodefinetheimpactthatmigratorygeesehaveonwatersafetyandhumanhealthbystudyingmigratorygeeseatSilverLakeinRochester,MN.Bothculture-dependentand-independentmethodswereusedtoanalyzegenotypesofCampylobacterfromwaterandgoosefecalsamplescollectedatSilverLake.IsolatespositivefortheCampylobacterflaAgeneweresequenced,andaphylogenetictreewasassembledinordertodeterminehowtheCampylobacterchangedwithtime.TheflaAfragmentswerealsoamplifiedfromDNAdirectlyextractedfromwaterandgoosefecalsamples.TheseflaAfragmentswillbesequencedusingNextGenerationSequencinginthenearfuture.

Presenter: EstherRodmanPosterNumber: 48HomeInstitution: MacalesterCollegeProgram: LSSURPFacultyMentor: Dr.LisaPetersonResearchAdvisor: RashiAroraPosterTitle: ExpressionAnalysisofGSTT1andEPHX1inHapMapCellsAbstract: 1,3-butadiene(BD)isclassifiedasaknownhumancarcinogenbytheNational

ToxicologyProgram,basedonitslinktoleukemiainexposedworkersandlaboratoryanimalstudies.Humanexposureoccursthroughtobaccosmoke,carexhaust,andmanufacturingofstyrene-butadienerubber.Inthebody,P450catalyzestheoxidationofBDintoreactiveepoxides.TheseepoxidesreactwithDNAtocreateDNAadducts,whichcanleadtomutationsandcancer.Detoxificationoftheepoxidemetabolitesoccursthroughconjugationwithglutathione,catalyzedbyglutathione-S-transferasetheta1(GSTT1)orthroughhydrolysis,catalyzedbyepoxidehydrolase1(EPHX1).ThefocusofthisstudyistocharacterizetheroleofGSTT1andEPHX1inpreventingthemutagenicityandtoxicityofBD.Toaccomplishthis,40humanHapMapcelllinesfromtwopopulations,fromNigeriaandUtah,willbeselectedforhighandlowexpressionofeachgene.ThisclassificationhasbeendoneinsilicobyfindingdataonGSTT1expressionfromthe1000GenomeDatabaseandonEPHX1expressionfromworkdonebyZhangetal(AJHD,2008).TheGSTT1genotypeandgeneexpressionofGSTT1andEPHX1willbeexperimentallydeterminedviaPCRandRT-qPCR,respectively,oneachofthe40celllines.TheseresultswillleadtotheidentificationoftheroleandinteractionofGSTT1andEPHX1inthemetabolism,detoxification,andsensitivityofBDwithinandbetweenhumanpopulations.

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Presenter: YanitzaRodriguez-GonzalezPosterNumber: 49HomeInstitution: UniversityofPuertoRico-MayaguezProgram: LSSURPFacultyMentor: Dr.TheodenNetoffResearchAdvisor: BrendaOglePosterTitle: StudyingtheCellularMechanismsofEpilepsyandCharacterizationofNeural

StemOrganoidsAbstract: Geneticanalyseshavediscoveredmanymutationsassociatedwithepilepsy,the

majorityofwhichareknowntoberelatedtosynapticfunction.However,amutationintheX-linkedgene,protocadherin19(PCDH19),isthoughttobeacalcium-dependentcell-adhesionprotein.Howthismutationresultsinepilepsyisnotknown.TheultimategoalofthisstudyistounderstandhowPCDH19affectsneuronalactivity.ThespecificgoalofthestudywastoidentifydifferencesinneuralactivityandanatomybetweenneuronalorganoidsculturedfromnormalcontrolsandepilepticpatientswithPCDH19mutations.WehypothesizedthatexpressionofPCDH19willbedecreasedinorganoidsgrownfrompatientswiththismutationandthattheactivityoftheorganoidswithPCHD19willbehyper-excitableinresponsetostimulationwithpotassiumandglutamate.Cellsweretakenfromhumansubjects,madeintopluripotentstemcellsandthendifferentiatedandculturedintocerebralorganoids.AnatomicalchangeswerestudiedusinghistologicalslicesoftheorganoidslabeledwithimmunohistologicalstainingofPCDH19,PCDH11,andPFAK.Theneuralactivitywasmeasuredusingcalciumimaging.Neuralorganoidswerestimulatedusinghighpotassiumandglutamate.ResultsshowthatPCDH19hasadecreaseinactivityinpatientslidesratherthanwildtype,andPCDH11remainedthesame.Glutamatesignalswerepossiblyfoundincalciumtransients,futurestudieswillbeconducted.

Presenter: EdarisRodriguez-IzquierdoPosterNumber: 50HomeInstitution: UniversityofPuertoRico-MayaguezProgram: LSSURPFacultyMentor: Dr.MargaretTitusPosterTitle: AUniqueDictyosteliumdiscoideumMyosinIsRequiredForChemotaxis

SignalingAbstract: Mitogen-activatedproteinkinases(MAPKs),betterknownasextracellular-signalregulated

kinases(ERKs)and(cAMP)signalingpathwaysareinvolvedinavarietyofcellularprocessessuchasproliferation,andchemotaxis.Theactivationofadenylylcyclaseisthemostcomplex,involvingG-proteinsandcomponentsoftheMAPkinasepathway.AuniqueDictyosteliumdiscoideummyosin,myoGthatisphylogeneticallydistinctfromunconventionalmyosinsandplaysacriticalroleincellpolarizationandchemotaxis.MyoGnullmutantcellsplacedinacAMPgradientarenoticeablyround,indicatingthattheyfailtopolarizeandmoverandomlywhenexposedtoachemotacticgradient.TheMAPkinaseERK2playsanimportantroleintheresponsetothechemoattractantcAMP.ItwasshownpreviouslythatDictyosteliumMAPkinaseERK2isrequiredfornormalactivationofadenylylcyclaseanderk2nullcellsareaggregation-deficient.ThesefindingssuggestMAPkinaseERK2israpidlyandtransientlyactivatedinresponsetothechemoat-tractantcAMPinthemyoGmutants.Thegoalofthisstudyisseeifachemotaxismutant(themyoGnullmutant)hasadefectisERK2activationfollowingcAMPstimulation.AnalysisofacollectionofchemotacticmyoGmutantsrevealsthatthemutantsaredefectiveinERK2activationfollowingcAMPstimulation.ThisdatasuggestthatmyoGisrequiredforERK2signalpathwaythatisrequirementforchemotaxissignalinginmyoGmutants.

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Presenter: PamelaRodriguez-VegaPosterNumber: 51HomeInstitution: UniversityofPuertoRico-MayaguezProgram: LSSURPFacultyMentor: Dr.KalpnaGuptaPosterTitle: MechanismofMastCellNuclearExtracellularTrapsAbstract: Sicklecelldisease(SCD)isaninheritedautosomalrecessiveblooddisordercharacterized

byinflammation,oxidativestress,ischemiareperfusioninjury,hemolysis,vaso-occlusivecrises,andpain.OurlaboratoryhasdemonstratedearlierthatmastcellactivationcontributestoinflammationandpainintransgenicmicewithSCD.Wehypothesizethatincreasedinflammationandfreehemereleasedduringhemolysisactivatesproteinargininedeiminase4(PAD4)inmastcellsleadingtonuclearextracellulartrap(NET)formation.WeareexaminingdifferentpathwaysthatactivatePAD4toseewhichinfluencedownstreamsignalingandNETformation.Wefoundthatco-incubationofmouseskin-derivedmastcellswithheminandTNF-αleadstomastcellNET(MCNET)formation.Silencinghigh-affinityIgEreceptor(FCεR1),whichstimulatesthetyrosinekinaseSYK,hasnoeffectoninhibitingTNF-α/hemininducedMCNETs.Weuseddifferentinhibitors,includingGSK484,aPAD4selectiveinhibitor,andImatinib,ac-kitinhibitor,toseetheireffectsonMCNETs.OurresultsdemonstratethatImatinibreducesthereleaseofTNF-αandGSK484reducestheformationoftrapsinactivatedmastcellsfromtheskinofsicklecellmice.

Presenter: AnneRofflerPosterNumber: 52HomeInstitution: ChapmanUniversityProgram: LSSURPFacultyMentor: Dr.AmeetaKelekarPosterTitle: DevelopingaNovelHighThroughputEnzymaticAssayforMalate

DehydrogenaseIAbstract: Increasedglucoseconsumptionandglycolysisisahallmarkofcancer.The

regenerationofNAD+,anessentialcofactorforglycolysis,hadbeenlargelyattributedtotheactivityoflactatedehydrogenase(LDH),whichconvertspyruvatetolactate.However,diversionofglucoseforbiosynthesistosupportproliferationreducescarbonsupplytoLDH.Thus,cancercellsmustrelyonalternativepathway/storeplenishNAD+forsustainingglycolysiswhileenablingbiomasssynthesis.RecentstudiesfromtheKelekargrouprevealedthatcytosolicNAD+isalsoreplenishedbymalatedehydrogenaseI(MDH1)throughconversionofoxaloacetatetomalate.AsproliferatingcancercellsrelyonbothLDHandMDH1activity,inhibitionofbothenzymespromisestobeaneffectivetherapeuticapproachagainstthesecancers.ToidentifysyntheticinhibitorsthatarehighlyspecifictoMDH1,andnotMDH2,anovelandsensitivehighthroughputassaywasdevelopedtomeasureMDH1activity.TheassaycocktailcontainsoxaloacetateandNADH,thetwosubstratesforMDHactivity,andeitherinvitrotranslatedFLAG-taggedMDH1orpurifiedhumanrecombinantMDH1orMDH2.ThereadoutforactivityisoxidationofNADHtoNAD+,measuredbylossofabsorbanceat340nmovertime.SubstrateconcentrationswereoptimizedthroughextensiveMichaelis-Mentenkineticswhileenzymeconcentrationandincubationtimewereadjustedthroughkineticconcentrationgradients.TheresultsofthisstudywilllaythefoundationforahighthroughputscreenforsmallmoleculeMDH1inhibitorsthatcanpotentiallybeadministeredincombinationwithLDHinhibitiontopreventtumorprogression.

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Presenter: RobertRosenblattPosterNumber: 53HomeInstitution: UniversityofAlbanyProgram: LSSURPFacultyMentor: Dr.AnjaBielinskyPosterTitle: CDC45KnockoutusingCRISPR/Cas9Abstract: CDC45ispartoftheCDC45:Mcm2-7:GINS(CMG)helicasecomplexrequiredforDNA

replication.Itinteractswithseveralotherreplicationfactors,includingtheminichromosomemaintenance10(MCM10)protein.MCM10isessentialandinvolvedinhelicaseactivation.A~50%decreaseinMCM10duetotheablationofoneofthetwocopiesofthegenehasbeenpreviouslyshowntocausetelomereerosionintransformedcelllines,leadingtocelldeath.Therefore,establishingtheexactmechanismbywhichtelomereshorteningoccursisofkeyimportance.ThegoalofthisprojectwastogenerateaheterozygousCDC45+/-celllinetodetermineifthetelomereerosionphenotypeofMCM10+/-cellscanbemimicked.AcomparisonbetweenthetwocelllineswillallowustoassessiftelomeremaintenanceisonlyreliantonMCM10oronotherreplicationproteinsaswell.UtilizingtheCRISPR/Cas9knockoutsystem,weknockedoutonealleleofCDC45,andthenplannedtouseTRF(TelomereRestrictionFragment)analysistodeterminewhethertheheterozygousCDC45celllinealsodisplaysshorttelomeres.Regardlessoftheoutcome,thiscomparisonwillbeinformative.IfasetofproteinsortheMCM10proteinaloneisestablishedasthecauseoftelomereerosionintransformedcells,aneffectiveproteininhibitorcouldbedevelopedthatmayworktooverridetelomeraseactivityincancercells,thusdrivingthesecellstokillingthemselves.

Presenter: MarioSoto-SotoPosterNumber: 54HomeInstitution: UniversityofPuertoRico-MayaguezProgram: LSSURPFacultyMentor: Dr.RobertTranquilloPosterTitle: Effectoffibrinsourceondevelopmentoftissueengineeredvasculargraft.Abstract: Understandinginteractionsofthehumanbodywithbiomaterialsiskeytoexperimental

designintissueengineeredvasculargrafts.Fibriniscurrentlyusedasscaffoldmaterialforvasculargraftmodeling.Thefibrinmoleculeisbiodegradableandsuitableforcellremodeling.Humanfibrinandbovinefibrinareplacedunderanalysisinthisexperimentforthefirsttimeinourlabtocomparebiochemicalandmechanicalpropertiesthatareofimportanceforbloodvesselconstruction.Preliminarydataindicatespositivebiochemicalandmechanicalpropertiesinvitroforbovinefibrin.Cellviabilityisobservedinconstructswithbovinefibrinandhumandermalfibroblast.Humanfibrin(Baxter)isusedtobuildasimilarconstructtothebovinemodel.Thehumanmodelexhibitssamebiochemicalandmechanicalpropertiesattheinitialphase,withoutcellsinmatrix.Whencellswereaddedtothehumanbovineconstruct,adecreaseinvessellengthwasobservedcontinuouslyfromday3today14ofincubation.Thefibrinmodelofbovineconstructremainedstableexhibitinganincreaseincelldensity.Vascularlikeanatomicalfeatureswereobservedinthebovinemodelbutnotinthehumanmodel.Incontrast,anincreaseofcollagenproductionbythecellswasobservedinthehumanfibrinscaffold.Optimaltensilestrength,maximumtensionandmembranestiffnessfavoredthehumanfibrinconstructoverthebovine.Vesselshrinkingisattributedtothefactthatcellsproducemorecollageninthehumanconstruct.Newprotocolsarebeingestablishedinordertodevelopbloodvesselsusinghumanfibrinwhileconservingnativeanatomicalfeatures.

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Presenter: SarahSt.PierrePosterNumber: 55HomeInstitution: WorchesterPolytechnicInstituteProgram: LSSURPFacultyMentor: Dr.VictorBarocasResearchAdvisor: JuliaQuindlenPosterTitle: AFinite-ElementModelofWaveTransmissionandVibrotactileSensinginthe

FingerAbstract: ThePaciniancorpuscle(PC)isknowntoplayacentralroleinvibrotactilesensing,

butthedetailedmechanicalandneurologicalresponseofthefingertovibratorysurfacestimuli,mediatedbythePCs,hasyettobecompletelymodeled.Icreateda3Dfiniteelement(FE)modelofthehumanfingercomprisedoflayersfortheepidermis,dermis,subcutaneousandbone.Then,IembeddedPCsinanatomicallycorrectlocationswithinthemodel.Finally,IdevisednumericalexperimentstotesttheoutputofmymodeltovariousstimulibothwithandwithoutincorporatingPCsandcomparedmyresultstoseveralpublishedstudies.Mymodelcloselyreplicatesthebehaviorofahumanfingerasdemonstratedbydisplacementpatternssimilartohumanexperimentalandvalidatedmodelpublications.Ihavedeterminedthattheinclusionofmultiplelayersofskin,notablytheepidermis,affectstheresultsofthemodel.Assuch,a3DFEmodelwithaccuratemechanicalpropertiesandacomplexviewofthefingerisnecessarytoimprovemodelsofthePC.ThisresearchpresentsanovelmodelofmultiplePCsina3DFEfingeranaloguethatcanreplicateanddemonstratethecorrectresponseofthePCsandthefingertostimuli.

Presenter: HelenStreffPosterNumber: 56HomeInstitution: UniversityofNotreDameProgram: LSSURPFacultyMentor: Dr.ScottDehmPosterTitle: InhibitionoftheAndrogenReceptorN-terminalDomaininCastration-

ResistantProstateCancerAbstract: Prostatecancerclaims26,000Americanliveseachyeardespiteits99%5-yearsurvival

rate.Theandrogenreceptor(AR)actsasanimportanttranscriptionfactorinprostatecancer.Thus,therapiesformetastaticprostatecancertypicallyaimtoinhibittheARthroughchemicalandrogendeprivation.However,androgendeprivationisnotcurativebecauseprostatecancercellscanbecomeresistanttosuchtherapiesandprogresstocastration-resistantprostatecancer(CRPC).InCRPC,ARalternativesplicingoccurs,givingrisetoARvariantsthatlacktheligandbindingdomain(LBD).BecausetheseARvariantsretainthetranscriptionallyactiveN-terminaldomain(NTD),inhibitingtheARNTDmaybeamorepromisingapproachfordevelopingnewtherapeutics.Ahigh-throughputscreenof100,353compoundsledtotheidentificationoffourpotentialinhibitorsoftheARNTD.CellgrowthinhibitionbythesecompoundswastestedusingcrystalvioletandsoftcolonyformationassaysontwoprostatecancercelllineswhicharedrivenbytheARorARsplicevariants(LNCaPand22Rv1,respectively).Ascontrols,wetestedtwoprostatecancercelllinesthatlackexpressionoftheAR(PC-3andDU145).TheresultsindicatedthatthreeofthesecompoundssuccessfullytargettheAR,mostlikelythroughinhibitionoftheNTD.AdditionalstudiesarewarrantedtocharacterizetheARNTDspecificityofthesecompounds,whichcouldleadtonewtherapiesthatimprovethelivesofmenwithadvancedCRPC.

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Presenter: AidanTirpackPosterNumber: 57HomeInstitution: MacalesterCollegeProgram: LSSURPFacultyMentor: Dr.CraigHenkeResearchAdvisor: JeremyHerreraPosterTitle: DeterminingHyaluronan'sEffectOnIdiopathicPulmonaryFibrosisAbstract: IdiopathicPulmonaryFibrosis(IPF)isaprogressivelungdiseaseofunknowncausewithfew

treatmentoptions.Ithasaprevalenceofonemillionpeopleworldwide.IPFisdefinedbytheaccumulationofextracellularmatrix(ECM)withinthelungthatleadstopatientdeathbyasphyxiation.IthasbeenpreviouslyreportedthatwhenfibroblastsareculturedondecellularizedIPF-ECM,ECMsynthesisisactivatedthroughthederegulationofmicroRNA-29(amasternegativeregulatorofECMsynthesis).WealsoshowthatthisderegulationisduetoDicer1(akeyregulatorofmicroRNAprocessingmachinery)suppressioninIPF.LeftunansweredisthemechanismbywhichIPFECMregulatesDicer1expression.Hyaluronan(HA)isahydrating,spacefillingpolymerthatisinvolvedwithinflammationandwoundhealingwithintheECM.HAhasbeenreportedtobeupregulatedinIPF,andHAhasbeenshowntoupregulatefibroblastcollagensynthesisbothinvitroandinvivo.However,thedirectlinkbetweenHAandDicer1hasnotyetbeendescribed.TodetermineifHAhasaneffectonDicer1wewillbetreatingfibroblastsincellculturewithvariousformsofHAundermultipleconditions.WehypothesizethatwithanincreaseinHAtherewillbeadecreaseinDicer1expression.Ifthisisthecase,thiscouldleadtonewtreatmentofIPF.

Presenter: ValeriaTorres-IrizarryPosterNumber: 58HomeInstitution: UniversityofPuertoRico-CayeyProgram: LSSURPFacultyMentor: Dr.DeepaliSachdevResearchAdvisor: KatelynHoff,MatthewMartienPosterTitle: CharacterizationOfANovelInVivoModelOfTamoxifen-ResistantBreast

CancerAbstract: ThemostcommontypeofbreastcancerdiagnosedintheUnitedStatesisestrogenreceptor

positive(ER+).ER+patientsaretreatedwithanti-hormonaltherapiessuchastheselectiveestrogenreceptormodulator(SERM)tamoxifen,whichinhibitstheeffectER.Nearly1/3ofthesepatientsdevelopresistancetohormonaltherapiesandrecur.ERandthetypeIinsulin-likegrowthfactorreceptor(IGF1R)signalingpathwayscommunicateandworktogethertostimulategrowthofbreastcancercells.DrugstargetingIGF1RandIRmayworkastreatmentforresistantcancercells.However,initialtrialswithIGF1Rdrugsindicatedapaucityofpreclinicalmodelsofendocrineresistantbreastcancers.TodevelopmoreclinicallyrelevantmodelstostudynewdrugcombinationsforER+patientsandunderstandthemechanismofresistancetotamoxifen,wepreviouslydevelopedandcharacterizedaninvitromodelofacquiredtamoxifenresistancebyculturingER+breastcancercelllineMCF-7Linincreasingconcentrationsoftamoxifen(MCF-7LTamRcells).Inthisstudy,wedevelopedaninvivomodeloftamoxifenresistancebygrowingMCF-7LTamRcellsasxenografttumorinthepresenceoftamoxifenbutnotestradiol.Theinvivotamoxifenresistantline,c287m1MCF-7L-TamR,wasestablishedfromtheMCF-7LTamRtumorfollowingcontinuedtamoxifenresistanceinvivofor100days.Herein,thislinewascharacterizedforcontinuedresistancetotamoxifen,IGF/insulinsignaling,andERregulatedgeneexpression.WefoundthatMCF-7LTamRxenografttumoraswellastheinvivotamoxifenresistantline,C287m1MCF-7LTamR,maintainedlossofIGF1RexpressionasmeasuredbyquantitativereversetranscriptionPCR(qRT-PCR)andwesternblotting.InvivotamresistantcelllinealsomaintainedresistancetotamoxifenandsignalingbyinsulinbutnotIGF-I,WeaimtocreateanewinvivomodeloftamoxifenresistancewheretargetedtherapiescanbedevelopedfortamoxifenresistantER+breastcancersoitcanbesuccessfullytreated.

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Presenter: JesusVazquezPosterNumber: 59HomeInstitution: UniversityofNewMexicoProgram: LSSURPFacultyMentor: Dr.NeilAndersonPosterTitle: StemWidth,DryWeight,AndChlorophyllLevelDifferencesInBrassicajuncea

AndB.OleraceaInSodiumChlorideAbstract: Highsalinityinsoilnegativelyaffectstheproductionoffoodcropsinagriculture.

Hydroponics,thecultureofplantsinnutrient-enhancedwaterwithoutsoil,canalleviatetheadverseeffectsofhighsalinityonthegroundaswellasotherissues,byofferingabettercontrolenvironment.Theobjectiveofthisresearchistounderstandtheeffectsofsodiumchlorideinplantsgrownhydroponicallytoaccessthepossibilityofusingwastewaterfrombreweriesandcreameriesinhydroponicsystems.Thisexperimentassessestherelativegrowthofstems,plantheight,leafnumber,andchlorophylllevelsinKale(B.oleracea)andmustardgreens(B.juncea)grownindifferentconcentrationsofsodiumchlorideinhydroponics.Fourdifferenthydroponicsystemswereused,eachonecontainingdifferentconcentrationsofNaCl:0ppm,50ppm,100ppmand200ppmfortwotrials;and0ppm,200ppm,400ppmand800ppmfortwoadditionaltrials.Allsystemscontainedthesamebasicnutrientsolutionforhydroponics.Dryweightdifferenceswerepresentwhenmustardgreenswereexposedto800ppmofNaCI.Atthislevel,mustardgreensweresignificantly0.33gramsheavierthanmustardgreensexposedtoonly100ppmofNaCI.

Presenter: EstherVega-QuiñonesPosterNumber: 60HomeInstitution: UniversityofPuertoRico-AreciboProgram: LSSURPFacultyMentor: Dr.MaximCheeranResearchAdvisor: VenkatramanaD.Krishna,WalterC.Low,LingLiPosterTitle: EffectsofM2MacrophagesonNeuroinflammationandNeurogenesisinAged

APP/PS1MiceAbstract: Alzheimer’sdisease(AD)isadebilitatingneurodegenerativedisorderresultingfrom

neuroinflammationandaccumulationofamyloid-βplaquesandneurofibrillarytangles.Alternativelyactivated(M2)macrophages/microgliahavebeenshowntoimpartneuroprotectiveeffectsbyreducingamyloid-βinducedinflammation.Inaddition,previousstudiesinthelaboratoryhaveshownthatM2macrophagesenhanceneurogenesisinmice.Inthepresentstudy,weexaminedwhetheradoptivetransferofM2macrophagesdecreasedinflammationandincreasedneurogenesisinatransgenicmurinemodelofAD(APP/PS1).Throughrandomassignment,7-8month-oldmicereceivedeitherM2macrophagesorsalineviaintra-peritonealinjection,3times/weekfor6weeks.AfterM2macrophagetreatment,changesininflammatorycellphenotypesandgeneexpressionwillbeanalyzed.ThefrequenciesofmacrophageactivationphenotypesinthebrainwillbedeterminedbyflowcytometryandgeneexpressionbyRT-PCR.WehypothesizethatadoptivetransferofM2macrophagesinagedmicedecreasesneuroinflammationandassociatedamyloid-βplaqueaccumulationinthebrainofagedmice.Inaddition,M2macrophagesareexpectedtoincreaseneurogenesisbyincreasingneuralstemcellnumbersandinducingdifferentiationintoneurons.UnderstandingtheroleofM2macrophageonneuroinflammationandneurogenesiscouldresultindevelopingnewtreatmentstodecreasetheeffectsofAlzheimer’sDisease.

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Presenter: LorenWeberPosterNumber: 61HomeInstitution: BereaCollegeProgram: LSSURPFacultyMentor: Dr.JulieGrossmanResearchAdvisor: VivianWautersPosterTitle: TheChangesinLabileCarbonBeforeandDuringSummerCoverCropGrowthAbstract: Anassessmentofsoilcarbondynamicsduringsummercovercropgrowth,via

comparisonofthelevelsoflabilecarbonbeforecovercropplantingandafter36daysofcovercropgrowthwithfourdifferenttreatmentsandtwobarecontrols.FourreplicationsweregrownonCalafarminTurtleLake,WIwitheachofthefollowingtreatments:1)chicklingvetchandsorghum-sudangrass,2)cowpeaandsorghumsudangrass,3)sunnhemp,4)buckwheat,5)twobarecontrols.SoilsamplesfromeachtreatmentweremeasuredforactivecarbonusingPOX-Clabassay,inwhichpotassiumpermanganateoxidizestheactivecarbonindrysoils.Labilecarbonlevelsatcovercropplanting(0day)werefoundtobesignificantlydifferentcomparedtolabilecarbonlevelsduringthesummercovercropgrowth(36days).Thedatashowedasignificantdifferenceinlabilecarbonlevelsbetweenthefourreplications,whiletherewasnosignificantdifferencebetweentreatments.Basedonthesesamplingtimepointslabilecarbonlevelsappeartobemoreaffectedbymanagementorseasonalfactorthanbycovercropgrowth.

Presenter: AmeliaWindorskiPosterNumber: 62HomeInstitution: SmithCollegeProgram: LSSURPFacultyMentor: Dr.PatrickRothwellPosterTitle: EstablishingSensitizationtoOxycodoneinWildTypeMiceAbstract: Oxycodoneaddictionimpactsthousandsofindividualswhobecomesensitized

tothemotivationaleffectsofdrugs.Underlyingthisenhancedmotivationarechangestotherewardsystem.Inmice,locomotorsensitizationisaproxyforobservingtheunderlyingchangestotherewardsystem.Thegoalofthisresearchwastodeterminehowdifferentmethodsofadministrationimpactoxycodonesensitization.CohortAwasadministeredoxycodone(0mg/kg,2.0mg/kg,6.32mg/kg,and20mg/kg)viasubcutaneousinjectiononceperdayforsevendays.CohortBwasimplantedwithoxycodone(0mg/kg,6.32mg/kg,20mg/kg,and45mg/kg)Alzetpumps.Ondaysoneandsevenallmiceweretestedforanalgesiaandlocomotion.After13daysofwithdrawal,micefromallgroupswerechallengedwithsaline,followedbyincreasingdosesofoxycodone.Miceonintermittentoxycodoneexhibitedlocomotorsensitizationonday7(p<0.0001)whilemiceoncontinuousoxycodonedidnot.Miceon20mg/kg/dayofintermittentoxycodoneexhibitedlocomotorsensitization(p<0.019)thatextendedafterwithdrawal.Theprojectshowedthatlocomotorsensitizationtooxycodoneoccurswithhigherdosesofintermittentoxycodoneandcanpersistovertime.Sensitization,resultinginchangestothebrainrewardsystem,reflectsabiologicalprocessthatcontributestoaddiction.Administrationthatdoesnotleadtosensitizationmayrenderindividualslesslikelytoabuseopioids.

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