Scientific Harrovian IX 1

Aboutthe

SCIENTIFIC HARROVIAN

2024

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Thisisapupil-ledpublicationthatliaiseswithstafffromtheScience Departmenttoproducearticlesandartworkthatdelveintothe newestdevelopmentsinScience.Weaimtoinformandeducateour fellowpupilstocurateinterestsinSTEMorbuildonpreexisting passions.

Amessagefrom

MS MCCROHAN

HeadofBiology

‘Everythingeverywherewecannotsee’isaveryfittingtitleforthiseditionoftheScientific Harrovian.ThescopeofthesearticlesprovesthatSciencereallydoestoucheverything, everywhere,andisforeveryone.Whetheryouwanttotakeabreakandreadaboutantilockingbrakesorsinkyourteethintodentalhygiene,thereissomethinginthiseditionto piqueyourinterest.Iwouldliketothankandcongratulatethewriters,editors,andillustrators foralltheworktheyhavedonethatwecannotsee.Theteamhasbeenrunpassionatelyby twoexceptionalpupils,ValerieHoandKevinWu,whohavemotivatedtheteamtoproduce well-researchedandwrittenpiecesacrossarangeofsubjects.TheartistictalentsofAlicia Wanandherteamhavemadethiseditionvisuallystunning;youcannothelpbutpickitup.I hopeeveryonewhopicksupacopyofthisScientificHarrovianiswowedbyboththe creativityandscientificendeavoursofallthecontributorstothisedition

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VALERIE HO

CurrentEditorinChief

WelcometoissueIXoftheScientificHarrovian This year’sthemeis‘EverythingEverywhereWeCannot See’.

MynameisValerie(Y12,Anderson)andassomeone withanacuteinterestinSTEM,Ilovedreading, editingandformattingthesearticlesaseachone bringsauniquetopictofurthercementour understandingofthescientificworld.Theserange fromprosthetics,themicrobiome,quantumphysics anddiseases.

Theteamhasworkedincrediblyhardtoproducehigh-qualitywritingandartworkandIwouldlike tothankeveryonefortheirdedication. AspecialthanksgototheHeadEditorswhohavehelped chaseuparticles,trackdeadlinesandformatthisissue.

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KEVIN WU

PreviousEditorinChief

Hi!MynameisKevin(Y13Sun),andI'mtheprevious Editor-in-chieffortheScientificHarrovian.Scienceisan ever-evolvingfield,graduallyuncoveredbytheworkof countlessresearchers.Asapre-medstudentanda scienceenthusiast,Iloveexploringcutting-edgescience, whetherit'sstemcelltherapy,quantumcomputing,or artificialintelligence.Throughmyrole,Ihopetoprovidea platformforstudentstoshareandexpresstheirlovefor science,andinspiremanyotherstoembracethe enchantmentofresearch.

MEET THE TEAM

OurHeadEditors,Writers,EditorsandArtists

ZOE WONG

BiologyHeadEditor

Hello, I am Zoe (Y13 Anderson), the Biology Head Editor Through my love for writing and scientific exploration, I enjoy navigating complex concepts with those around me. As a future doctor and researcher, I embrace the challenges that Biology presents, and I anticipate the advancements it can bring. I hope that the articles will fuel your curiosity to ask questions and contribute to the understandingoftheworldaround(andwithin)us Happyreading!

BIANCA MAK

MedicineHeadEditor

Hello!IamBianca(Y12Wu) Iamdelightedtobe the Medicine Head editor As an aspiring medic, biology, especially the human anatomy, is a passion of mine: I love the intricacies and complexities of bodily functions As a Head Editor, it was extremely intriguing to read and edit all of the articles and see how much effort the writers have put into writing their articles I hope you enjoy this edition of the Scientific Harrovian!

DANIEL KAN

TechnologyHeadEditor

Hello!IamDanielKan (Y12Shaftesbury),andI’m theTechnologyHeadforthisyear’seditionofthe ScientificHarrovian.Assomeonewhohasalways beenextremelypassionateaboutscience,aswell asanaspiringmedic,Ihavealwaysbeenintrigued byfascinatingnewtechnologies,especiallythose relatedtothehumanbodyandBiology.Through myroleasHeadEditor,Ihopetoinspirethenext generationofHarrovianscientists.Happyreading!

SEN YI MOK

PhysicsHeadEditor

Hi!IamSenYi(Y12Shaftesbury)andthePhysics Head Editor for this year As a passionate physicist and future engineer, I am fascinated by the realm of quantum mechanics and the intricacies of engineering design processes. As Head Editor, I hope to spread my passion for these fields through the latest edition of ScientificHarrovian!

ALICIA WAN

HeadArtist

Hithere!I’mAlicia(Y11ofWu).IloveBiology(andofcourse, theothersciences,butbiologyprevails),especiallywhenit comestofindingouthowdifferentcreaturesliveandwork together.It'slikeuncoveringthesecretsofahiddenworld!As theHeadArtisthere,Iwantedtomixthiscoolworldofbiology withasplashofart,makingourarticlesnotjustinformativebut reallyfuntodiveinto Ibelievelearningaboutlifeshouldbean adventureweallgettoenjoy Afterall,weonlyhave100years tolive,andlife'stoopreciousnotto!

WRITERS

KingsleyLui Year13 Churchill

CaitlynTang Year12 Anderson

AndrewHung Year12 Churchill WincyChan Year13 Keller

BrianYam Year12 Peel

EDITORS

AudreyLam Year11 Wu

GabuIwasaki Year6 Darwin

DavynKwok Year8 Darwin

IsabellaXu Year12 Wu

YiliaWang Year6 Parks

KatieOnyschenko Year9 Keller

ARTISTS

FloraChen Year11 Anderson

CynthiaLi Year11 Keller

Frontcover Backcover

JeffreyLing Year12 Peel

ZoeWong Year13 Anderson

CharlizeMui Year11 Wu

CathyShen Year6 Nightingale

CaitlynTang Year12 Anderson

BIOLOGY

How Behavior is Affected by The Gut Microbiome

By Wincy Chan

microorganisms,justliketheEarthishome ecollectivegenomesofmicroorganismsin biotaisdefinedasthecommunityof hesemicroscopicmicrobeshaveexistedin ecentlycometorealizetheirsignificance. compellinglinksbetweenhumanhealth shownthatalthoughthegutmicrobiotais uchasdrugsanddietmayheavily mposition[4].Inaddition,animalmodels onshipbetweenthegutmicrobiotaandthe gicaldiseases.Forexample,alower withinpeoplewithinflammatorybowel re,studyingthegutmicrobiomeingreater sofourlives,leadingtobettermentaland viourthroughbrainbiochemistry,are otaundergoesalterations.This,inturn, haviour[6].Thegut-brainaxis,atopicof es,hasrevealedbrainbiochemistry isphenomenon.Dysbiosis,animbalanced utmicrobiome,playsacriticalroleinthis iggerarangeofneurologicalproblemsand inthecomparisonbetweengerm-free(GF) ofmicrobesinanypartoftheirbody, behaviourwhensubjectedtostress. brainsofGFmicehadanaltereddopamine heregulationofstressandanxiety. adapttonewenvironments[2]. ngeneexpressionsrelatedtosurvivaland biosispassivelybygivingantibiotics. edtobemoreexploratory,butthis nthegutmicrobiotawasnormalised[1]. etingneurotransmittersand ancetheexcitatoryorinhibitoryresponses ane)[5]thatactongeneexpression,the sabilitytoadapttonewenvironmental croorganismsthatisestablishedinearlylife sthatleadtochangesinitsdevelopment nourgutcanhavebeneficialand leaveusfeelingasenseofnauseabefore developneurologicaldiseases[3].

rainandgutmicrobiomecommunicate andthisrelationshipiscrucialforregulating overallbehaviour.Byunderstandinghow hemicrobiome,wecantakestepsto tyoflife.

2.0 Bibliography

[1]Bercik,P.,Denou,E.,Collins,J.,Jackson,W.,Lu,J.,Jury,J.,Deng,Y.,Blennerhassett,P.,Macri,J.,McCoy,K.D., Verdu,E.F.andCollins,S.M.(2011).TheIntestinalMicrobiotaAffectCentralLevelsofBrain-DerivedNeurotropic FactorandBehaviorinMice.Gastroenterology,141(2),pp.599-609.e3. doi:https://doi.org/10.1053/j.gastro.2011.04.052.

[2]Crumeyrolle-Arias,M.,Jaglin,M.,Bruneau,A.,Vancassel,S.,Cardona,A.,Daugé,V.,Naudon,L.andRabot,S. (2014).Absenceofthegutmicrobiotaenhancesanxiety-likebehaviorandneuroendocrineresponsetoacute stressinrats.Psychoneuroendocrinology,42,pp.207–217. doi:https://doi.org/10.1016/j.psyneuen.2014.01.014.

[3]HarvardHealthPublishing(2019) Thegut-brainconnection [online]HarvardHealth Availableat: https://wwwhealthharvardedu/diseases-and-conditions/the-gut-brain-connection

[4]Kootte,R.S.,Levin,E.,Salojärvi,J.,Smits,L.P.,Hartstra,A.V.,Udayappan,S.D.,Hermes,G.,Bouter,K.E.,Koopen, A.M.,Holst,J.J.,Knop,F.K.,Blaak,E.E.,Zhao,J.,Smidt,H.,Harms,A.C.,Hankemeijer,T.,Bergman,J.J.G.H.M., Romijn,HA,Schaap,FG andOldeDamink,SWM (2017) ImprovementofInsulinSensitivityafterLeanDonor FecesinMetabolicSyndromeIsDrivenbyBaselineIntestinalMicrobiotaComposition CellMetabolism,26(4), pp.611-619.e6.doi:https://doi.org/10.1016/j.cmet.2017.09.008.

[5]Lentz,T.L.andErulkar,S.D.(2019).NervousSystem-NeurotransmittersandNeuromodulators.In: EncyclopædiaBritannica.[online]Availableat:https://www.britannica.com/science/nervoussystem/Neurotransmitters-and-neuromodulators.

[6]Shen,H.H.(2015).Couldthegutmicrobiomehaveacriticalroleinbrainandbehavior?Thenotionisstarting togainacceptanceamongstbothresearchersandfunders:Couldthegutmicrobiomehaveacriticalrolein brainandbehavior?Thenotionisstartingtogainacceptanceamongstbothresearchersandfunders. ProceedingsoftheNationalAcademyofSciencesoftheUnitedStatesofAmerica,[online]112(30),pp.9143–9145.Availableat:https://www.jstor.org/stable/26464155.

[7]Valdes,AM,Walter,J,Segal,E andSpector,TD (2018) Roleofthegutmicrobiotainnutritionandhealth BMJ:BritishMedicalJournal,[online]361.Availableat:https://www.jstor.org/stable/26961091.

What causes Alzheimer’s Disease?

By Zoe Wong

1 What is Dementia and Alzheimer’s Disease?

Dementiaisasyndrome,whichisacollectionofrecognisablesignsandsymptomsindicatingacondition wherethedirectcausemaynotbeknownyet.Itisnotonespecificdisease.Dementiamainlyaffectsadultswho are65yearsofageandolder,althoughthereareraregeneticdisorderscausingchildhooddementiasuchas Niemann-PickType-C.Dementiaisaprogressivedisease,whichmeanssignsandsymptomsmaystartmild andworsenwithtime;symptomsvarygreatlyandcanincludeproblemsassociatedwithmemory,attention, communication,judgement,personalitytraits,andvisualperception.Commonexamplesincludegettinglost, forgettingrecentevents,askingthesamequestionrepeatedly,losingbelongings,andhavingdifficulties performingfamiliartasks.Inseveredementiacases,agnosia(inabilitytorecogniseobjects)andapraxia (difficultycoordinatingmovements)maybeseen

Therearedifferenttypesofdementiasuchasvasculardementia,frontotemporaldementia,alcohol-related dementia,andmixeddementia.Themostcommontype,whichthisarticlewillfocuson,isAlzheimer’sDisease (AD),whichaccountsfor60%ofallcases.SporadicADorlate-onsetADaccountsforaround95%ofcases, whilstfamilialADorearly-onsetADaccountsforaround5%ofcases.Dementiaisnotanormalpartofageing. Unfortunately,asmanyas62%ofhealthcareprofessionalsworldwidebelieveitispartofthenormalageing process.

2 Causes of Alzheimer’s Disease

ScientistsdonotfullyunderstandwhatcausesAD;theyhaveonlyputforwardhypothesesthatexplainthe observedphenomena.Manyagreethatcurrenthypothesesdonotexplainthewholepicture,andmore researchneedstobedonetorevealmorewhatcausesAD.Thissectionisdedicatedtounderstandingfourof themainhypotheses:theAmyloidCascadeHypothesis,theTauHypothesis,theInflammationHypothesis,and theCholinergicHypothesis.

Figure 1. Dementia is an umbrella term. It is important to note that there are many types of dementia, and also dementia like diseases. They are not the same thing.

2.1 The Amyloid Cascade Hypothesis and Genetic Mutations

TheAmyloidCascadeHypothesisdatesbacktoJohnHardyandDavidAllsopwhofirstproposedthehypothesisin1991 Ithassincedominatedthefieldandfuelledthepursuitofanti-ADdrugsthattargetamyloidbetaplaques Itisimportantto notethat‘Aβ’and‘amyloid’arenotsynonymousterms;amyloidreferstoaggregatesofanytissuefibrilswithspecific properties,whilstAβrefersexclusivelytotheproteinthatcanaggregatetoformaspecifictypeofamyloidassociatedwith AD.

Accordingtothishypothesis,ADisduetotheformationofplaquesfromaccumulatingAβpeptidesorAβmonomers outsidetheneurone.Thesepeptidesderivefromtheamyloidbetaprecursorprotein(APP).APPisanintegralprotein whichishighlyconcentratedinthesynapsesofneuronesandcanalsobefoundinmanytissuesinthebody.Itisfound embeddedinthecellmembrane,andalthoughit’sfunctionisunknown(somebelieveitactsasacellsurfacereceptor), likemanyotherproteinsitgetsbrokendownandrecycled.Whenitiscleavedbytheenzymeα-secretaseintheβamyloiddomain,itisnotproblematic.However,whenitiscleavedbyβ-secretaseorγ-secretaseenzymes,thepeptides releasedareneurotoxicandcanaggregatetoforminsolubleamyloidplaques.Oneform,amyloid-beta42(Aβ42),isthe mostamyloidogenic(mostlikelytoresultintheformationofamyloidstructures)andisextremelyneurotoxic.Aβ monomerscanaggregatetoformoligomersandvariousfibrils,andthesefibrilsfurtherassembleintoamyloidplaques.

Thehypothesissuggeststhatamyloidplaquesinthesynapsesofneuronescandisruptsignallingandimpairbrain function,whichleadstothecharacteristicsymptomsofAD.Amyloidplaquescanalsodepositwithinthetunicaadventitia andtunicamediaofvesselsinthebrain,causingamyloidangiopathy,whichincreasestheriskofrupture,haemorrhage, andultimatelycontributestotheprogressionofAD.

Figure 2. The APP protein is cleaved by several enzymes. When cleaved by β-secretase and γsecretase, it releases neurotoxic Aβ peptides that can aggregate to form many oligomer species, fibrils, and fibrils that eventually form amyloid plaques. Certain mutations increase the activity of β-secretase and γ-secretase which implies possible genetic predisposition to AD.

Therehavebeenseveralgenesassociatedwiththishypothesis Thee4alleleoftheapolipoproteinEgene(APOEe4)isa strongriskfactorfordevelopingAD:carryingoneAPOEe4allelemeansa3to4timeshigherriskofAD;carryingtwois associatedwith10to15timeshigherriskofAD.APOEhelpsbreakdownplaques,butthee4isalesseffectiveallele,and thisleadstoearlyaccumulationofamyloidplaques,especiallyinhomozygouscarrierswhohavethegreatestAβburden. FamilialgenemutationssuchasPSEN-1andPSEN-2thatcodeforthesubunitsofγ-secretaseenzymeschangesthe locationwheretheenzymecleavesAPP.ThisleadstoAβmoleculesthatarebetteratformingplaques..Thegene encodingAPPliesonchromosome21,whichisthesamechromosomewherepeoplewithDownsyndromehaveextra geneticinformation.AutopsiesrevealedthatmostDownsyndromepatientshaveamyloidplaquesbythetimetheyare 30,andtheygoontodevelopADintheir40s6.ThisispossiblyduetoincreasedexpressionofAPPwhichmeans increasedamountsofamyloidplaques.

Therearealsoobservationsandstudiesthatdonotsupportthehypothesis.Brainautopsieshaveshownthesamelevelof amyloidmakeupinthebrainsofpeoplewithoutADwithpeoplewhodidhaveAD.LargeamountsofAβwasfoundinone thirdofcognitivelynormalolderadults.Decadesofresearchandclinicaltrialstargetingamyloidplaqueshaveproved unfruitful:since2018,12drugshavefailedinphaseIIIofclinicaltrials,with9ofthemtargetingamyloidplaqueformation directly.Therearecurrentlyonlytwoapproveddrugsthattargetamyloidplaques,lecanemabandaducanumab.Itis highlylikelythatthecascadehypothesisisnotanisolatedpathway,butratheronecomponentofamultifactorial condition.MoreresearchmustalsobedonetodeterminewhysomepatientswithamyloidlevelsashighasADpatients experiencenosymptomsanddonotshowanonsetofdementia.

Figure 3. Hashed circles refer to Aβ plaques; arrow points to a neurofibrillary tangle (NFT) (discussed in the following section) B. Bielschowsky’s silver stain of the dorsolateral frontal cortex showing amyloid plaque (hashed circles) and NFT (arrow) C Red Staining of amyloid plaques D Amyloid plaques; birefringence with cross-polarized illumination E Amyloid plaque F NFT

2.2 Tau Hypothesis

Anotherwell-knownhypothesisistheTauHypothesis,whichfocusesonagroupofproteinscalledtauproteins They cause‘tauopathies’,whichareneurodegenerativedisordersduetotheaggregationofmisfoldedtauproteins

Tauareassociatedwithmicrotubules,apartofacell’scytoskeleton,andimportantinmaintainingtheshapeofneurones andtransportingnutrientswithinneurones.ThereisstrongevidencesuggestingthatthefirstpathologicaleventinADis thedepositionofamyloidplaqueswhichthentriggerstheactivationofenzymestauproteinkinasesIandII.Thisiswhy ADisknownasa‘secondarytauopathy’,asthetaupathologyisdrivenbyAβ(seeFigure5)whichalsomeansitformsa positivefeedbackloop.Thekinasesareresponsibleforthehyperphosphorylationoftau,causingmicrotubulesto disassemble,allowingtaumoleculestoaggregateintofilamentscalledneurofibrillarytangles(NFTs),asshowninFigure 4.Scientistsusedtobelievethetauhypothesiswasrestrictedtothecytoplasmofneurones,butthishasbeenchallenged bystudiesshowingthepresenceoftauinextracellularfluidssuchascerebrospinalfluid(CSF),interstitialfluid(ISF),and bloodplasma.

Figure 4. The neurone on the top is a healthy neurone where the tau proteins help to maintain structural integrity. However, in the neurone of a person with Alzheimer’s Disease, tau is hyperphosphorylated, causing the microtubules to disassemble forming NFTs.

Figure 6. There are several types of NFT tangles: pre-tangles (a), early NFTs (b, e), typical NFTs (c, f), and ghost tangles showing remaining fibrils after disintegration of the neurone (d, g)

Figure 5. Serial sections of AD hippocampus. The top section is immunostained with an antibody to Aβ peptide The bottom section is immunostained with an antibody to hyperphosphorylated tau protein. Notice the foci of tau labelling (bottom section) corresponding to the same areas as the Aβ peptide (top section): they are amyloid plaque- associated nerve cell processes containing tau, implying relationship between Aβ and tau.

Neurofibrillarytanglesareneurotoxicandtheycauseneuronestodie,breakingneuralcircuitsandconnectionsof neuroneswhichcausesthesymptomsofAD.Tauhyperphosphorylationcanbeattributedtoseveraletiologicalfactors, suchasthepresenceofAβ,dysregulationofphosphorylation,andimpairedbrainglucosemetabolism.Mutationsinthe microtubule-associatedproteintau(MAPT)genethatcausesfrontotemporaldementiawithParkinsonismalsoshowhow taucouldleadtoneurodegeneration.

2.3 Microglial cells and the Inflammation Hypothesis

Microglialcellsarenon-neuronal,immunecellsinvolvedinthemaintenanceofcentralnervoussystemtissue They eliminatemicrobes,misfoldedproteins,anddamagedcells Microglialcellsarealsoinvolvedinsynapticpruning,where extrasynapticmaterialisengulfedtoensureactivesynapsesarestrengthenedwhilstredundantsynapsesareremoved Thishasaprotectiveeffectattheinitialstagewhereneurotoxicproteinaggregates,asmicrogliacancleartheseproteins viamicroglialphagocytosisandbyreleasingproteases

However,inlatestageAD,thebuild-upofAβandNFTscanaltertheneuroprotectiveeffectofmicrogliatoaneurotoxic effect Thisleadstoreleaseofproinflammatorycytokines,causingover-pruning,andinhibitionofsynapticplasticity, whichcontributestothesymptomsofAD

Thereleaseofproinflammatorycytokinesleadstoastateofchronicinflammationofthebrain.Thesecytokinesattract peripheralmacrophagesthattrytoclearamyloidplaques,butthisisbelievedtoexacerbateinflammationandAD pathology.NeuroinflammationisalsoassociatedwithdiseasessuchasParkinson’sdiseaseandamyotrophiclateral sclerosis.Aslow-actinganti-inflammatorysystemoranimbalanceofproinflammatoryandanti-inflammatorycytokines couldleadtoinflammationwhichexacerbatesAD.

2.4 Cholinergic Hypothesis

Cholinergicneuronesplayanimportantroleinlearning, memory,andattention,andareneuronesthatcontain acetylecholine(ACh) Whenpresynapticcholinergic neuronesaredepolarized,voltage-gatedcalcium channelsopen,allowingcalciumionsintothe cytoplasm Thisstimulatesthereleaseofthe neurotransmitterACh:theybindtoreceptormolecules inthepostsynapticneurone AChmoleculesdiffuse throughthesynapticcleftwheretheeffectisterminated, andAChisrecycledwhenmetabolisedbyhuman acetylcholinesterase(AChE)intocholineandacetic acids Cholineenterstheneuronethroughcholine transportersinthepresynapticneurone,andbindsto themetaboliteAcetylCoAtoformnewAChmolecules. Thecholinergichypothesisproposesthedegeneration ofcholinergicneuronesandseveredeficienciesofACh leadtoAD,andthesearefrequently-seenobservations inthebrainsofADpatients.

Figure 7. 1) Calcium ions enter through voltage gated channels which causes ACh to be released from vesicles. 2) ACh diffuses across the synaptic cleft and attaches to ACh receptors in the post-synaptic neurone that opens channels to allow sodium ions to flow into muscle cells. 3) AChE breaks ACh down into choline and acetate, and choline is used to make more ACh in the presynaptic neurone

3 Conclusion

Itisimportanttoappreciatetheindividualhypothesesastheyareusefulatguidingthedevelopmentofdrugsand diagnostictechniques,butweshouldnotforgetthatAlzheimer’sDiseaseisacomplex,multifactorialsyndrome, necessitatingaholisticapproachandconsiderationofallcontributingfactors

Moreresearchneedstobecarriedouttogainabetterunderstandingoftheinterrelationshipsbetweenthehypotheses, andtodetermineeffectivestrategiesforearlydetection,prevention,andtreatmentofAlzheimer'sdisease.

4 Bibliography

[Figure1]Alzheimer'sAssociation(2024) WhatIsDementia?[online]Alzheimer’sDiseaseandDementia Availableat: https:.alz.org/alzheimers-dementia/what-is-dementia.

Figure2]Patterson,C.,Feightner,J.W.,Garcia,A.,Hsiung,G.-Y..R.,MacKnight,C.andSadovnick,A.D.(2008).Diagnosisandtreatment ofdementia:1 RiskassessmentandprimarypreventionofAlzheimerdisease CanadianMedicalAssociationJournal,[online]178(5), pp.548–556.doi:https://doi.org/10.1503/cmaj.070796.

Figure3]Moncaster,J.A.,Moir,R.D.,Burton,M.A.,Chadwick,O.,Minaeva,O.,Alvarez,V.E.,Ericsson,M.,Clark,J.I.,McKee,A.C.,Tanzi, RE andGoldstein,LE (2022) Alzheimer’sdiseaseamyloid-βpathologyinthelensoftheeye ExperimentalEyeResearch,[online] p108974 doi:https://doiorg/101016/jexer2022108974

Figure4]Aging.,A."Alzheimer’sD.E.andR.C.,aserviceoftheNationalInstituteon(n.d.).English:Diagramofhowmicrotubules desintegratewithAlzheimer’sdisease [online]WikimediaCommons Availableat: https://commonswikimediaorg/wiki/File:TANGLES HIGHjpg

Figure5]ClinicalGate.(2015).Dementias.[online]Availableat:https://clinicalgate.com/dementias[Accessed20Mar.2024].

Figure6]Uchihara,T (2014) Pretanglesandneurofibrillarychanges:SimilaritiesanddifferencesbetweenADandCBDbasedon molecularandmorphologicalevolution.Neuropathology,34(6),pp.571–577.doi:https://doi.org/10.1111/neup.12108.

Figure7] Stanciu,GD,Luca,A,Rusu,RN,Bild,V,BescheaChiriac,SI,Solcan,C,Bild,W andAbabei,DC (2019) Alzheimer’s DiseasePharmacotherapyinRelationtoCholinergicSystemInvolvement Biomolecules,[online]10(1),p40 doi:https://doi.org/10.3390/biom10010040.

Dementiafactsheet (2023) wwwalzintorg [online]Availableat:https://wwwalzintorg/resource/dementia-fact-sheet/ CentersforDiseaseControlandPrevention(2019).WhatIsDementia?[online]www.cdc.gov.Availableat: https://wwwcdcgov/aging/dementia/indexhtml#: :text=Dementia%20is%20not%20a%20specific medlineplus.gov.(2022).APPgene:MedlinePlusGenetics.[online]Availableat: https://medlineplus.gov/genetics/gene/app/#: :text=Little%20is%20known%20about%20the. Chen,Z-R,Huang,J-B,Yang,S-L andHong,F-F (2022) RoleofCholinergicSignalinginAlzheimer’sDisease Molecules,[online] 27(6),p.1816.doi:https://doi.org/10.3390/molecules27061816.

Ishida,K,Yamada,K,Nishiyama,R,Hashimoto,T,Nishida,I,Abe,Y,Yasui,M andIwatsubo,T (2022) Glymphaticsystemclears extracellulartauandprotectsfromtauaggregationandneurodegeneration JournalofExperimentalMedicine,[online]219(3) doi:https://doi.org/10.1084/jem.20211275.

Griffiths,J andGrant,SGN (2022) SynapsepathologyinAlzheimer’sdisease SeminarsinCell&DevelopmentalBiology [online] doi:https://doiorg/101016/jsemcdb202205028

Our human body is extremely complicated. Many different organ systems work simultaneously to constantly supply our cells with oxygen and nutrients to keep us alive and running; the digestive system helps break down the food we eat, and the respiratory system provides a way for oxygen to be quickly delivered to the cells deep inside our body. However, one of the most crucial systems that we often only care about when we get the flu, or a cold is the immune system. An intricate system involving many specialised cells and proteins to rapidly adapt and protect our bodies against any foreign intruders from entering.

Our immune systems have had millions of years of evolution, fighting constantly against pathogens such as bacteria and viruses who constantly mutate in order find new ways to infect us with a nasty disease. Every cellular and protein interaction required to defend our body is fascinating but also absurdly complex and there is no way I can do it any justice within this article alone; a lot of the details will be missed out for simplicity purposes. That said, let’s delve into how your body will react when a virus tries to infect your cells and replicate to repeat the process.

Before we begin, what is a virus? A virus is considered a sub-microscopic infectious agent that replicates only inside the living cells of an organism, also known as a parasite. It is only made up of a few strands of RNA or DNA surrounded by a protein shell known as the capsid to enclose its genetic material. Finally, the virus is encased in and lipid bilayer envelope with protein spikes (receptors) atop those layers

Virusesarepathogenic,meaningtheycancausediseases,andtheyoftendothatbyinfectingthehost,enteringthecells andreprogrammingthegeneticmaterialofthecelltoproducemorevirusesandtoself-destruct.Thiscausesan exponentialgrowthofviruseswhilstkillingyourbodilycellsastheymovefromonecelltothenext.

Forobviousreasons,yourbodydoesnotwanttojustsimplyletthesevirusestearyourbodyapart,sothroughmanyyears ofevolutionithasdevelopedasystemtoprotectyourbodyfromtheseviruses(alongwithotherpathogenic microorganisms).ThissystemisknownastheImmuneSystem,anditiswell-coordinatedbysomeofyourorgans,white bloodcellsandrandomproteinsthatseeminglydriftinyourbloodvesselswithoutpurpose.

Sohowdoesyourbodystopavirusfromcausingtoomuchcollateraldamagewithinit?Thefirstlineofdefenceagainst thesevirusesarethephysicalbarriersprovidedbytheskin,gastrointestinaltract,nasopharynxandthemucous membranesintherespiratorytract. Theepithelialcellsthatlinethemucousmembranessecretemucuswhichtrap bacterialandviralpathogens,whichwouldthenbepusheduptothebackofthethroatbytheciliatedepithelialcells whereitcanbespatoutordigestedinthestomach.Thesecellscanalsoactivateandrecruitinnateimmunecellsby sendingoutchemokinesandcytokinestodendriticcells.

Figure1:Structureofavirus

Itisimportanttonotethatsomevirusesenterthebodythroughothermeans,suchasingestionordirectcontactwith infectedbodyfluids,butotherphysicalbarriersareinplacetheretopreventvirusesfrominfiltratingthebodyfromthere. Nonetheless,virusescansurpassthemandenterthebody.

Oncethevirusgetsintothehost’sbody,itwilltravelalongthesurfacesofthecellstoenteracelltoreplicateandreproduce morecopiesofitself.Generally,thereceptorsontheviruswillbindwith thecellviathenon-endocyticroute,causingthevirustofusewiththe cellandallowingtheDNAorRNAofthevirustoalterthegenetic informationofthecell.There,thevirususesthecellularmachineryto replicateandproducemorecopiesofitself,leadingtothespreadof infectiononcethenewvirusesbegintospreadtonearbycellswhere thecyclerepeats.

Thefirstresponsetoaviralinfectionistheinnateimmuneresponse.Itis “nonspecific”inthewaythatitrespondsinthesamewaytoallviruses andotherforeignsubstances,anditactsextremelyquickly,often detectinganddestroyingtheminhours.

Theresponseinvolvesquiteafewmechanisms: Onceacellisinfected,itbeginsproducingandreleasingsignalproteins knownasinterferons(typeofcytokine)Theseinterferonsbindtothe interferonreceptorsofnearbyuninfectedcells,wherethecellsbeginto produceanti-viralproteinsfromwithintohinderthespreadofthevirus tothosecells.Interferonsalsoinducenearbycellstoproducemajor histocompatibilityclassImolecules(MHCClassI).Thesemolecules presentviralantigenstootherinnateandadaptiveimmunecells.

Figure3:Methodsforviralentryintoacell

Figure2:EpithelialcellsintheImmuneSystem

Usually,cellshaveenoughMHCClassImoleculesfortheTcells,anadaptiveimmunecell,torecognisethemiftheydoget infected.However,virusescaninhibittheMHCclassIantigenpresentationpathway.Specialisedlymphocytes,suchasthe NaturalKillercells(NKcells)candetectwhenaninfectedcellhasdeficientamountsofMHCClassImoleculesandwould releasecelldeath-inducingenzymeslikegranzymesorperforin,killingthevirusinfectedcell.NaturalKillercellscanalso alertandattractotherimmunecellsthroughthereleaseofcytokines,oftensummoningthephagocytestocomeontothe battlefieldtofightagainsttheinfection.

Tostopthepathogenfromspreadingtoothercells,macrophagesingestthefreevirusesthroughaprocessknownas phagocytosis,whereitsurroundsandengulfsthevirusandsecretesdigestiveenzymesfromthelysosometobreakdown thevirus.Macrophagescanalsopresenttheantigensofthevirusithadingestedtootherimmunecells.Similarly,dendritic cells,likemacrophages,canpresenttheantigenstootheradaptiveimmunecells,buttheyaremorespecialisedin communicatingbetweentheinnateandadaptiveimmuneresponse.

Usually,cellshaveenoughMHCClassImoleculesfortheTcells,anadaptiveimmunecell,torecognisethemiftheydoget infected However,virusescaninhibittheMHCclassIantigenpresentationpathway Specialisedlymphocytes,suchasthe NaturalKillercells(NKcells)candetectwhenaninfectedcellhasdeficientamountsofMHCClassImoleculesandwould releasecelldeath-inducingenzymeslikegranzymesorperforin,killingthevirusinfectedcell NaturalKillercellscanalso alertandattractotherimmunecellsthroughthereleaseofcytokines,oftensummoningthephagocytestocomeontothe battlefieldtofightagainsttheinfection

Tostopthepathogenfromspreadingtoothercells,macrophagesingestthefreevirusesthroughaprocessknownas phagocytosis,whereitsurroundsandengulfsthevirusandsecretesdigestiveenzymesfromthelysosometobreakdown thevirus.Macrophagescanalsopresenttheantigensofthevirusithadingestedtootherimmunecells.Similarly,dendritic cells,likemacrophages,canpresenttheantigenstootheradaptiveimmunecells,buttheyaremorespecialisedin communicatingbetweentheinnateandadaptiveimmuneresponse.

Whenthebodycellsaredamaged,theyreleasechemicalsincludinghistamine,bradykinin,andprostaglandinswhich causethebloodvesselstoleakfluidsintothetissues,otherwiseknownasinflammation.Asirritatingasswellingcanbeto us,inflammationisextremelycrucialinsupportingourbody’simmunesystem:thefluidstopsthevirusesfromspreading elsewhereinyourbody,theycanalsohelpremovedeadtissuesfromthebattleground,andcanalsoallowimmunecells fromacrossthebloodstreamtotraveldirectlytothesiteofinfectiontohelpsupporttheotherinnateimmunecells.

Behindallthemainscenesinvolvingphagocytesandcytokines,arethecomplementarysystem.Oneoftheleastwellknownpartsoftheimmunesystem,itinvolvescountlessdifferentproteinsthatdriftinthebloodstreamfornopurposeatall, butwhenactivateditbecomesoneofthemostsophisticatedweaponsthatthebodyhasagainstinfections.Althoughthe complementsystemismoreeffectiveagainstbacteriaandotherpathogenicmicroorganisms,italsoplaysquitealargerole inquellingthespreadofviruses.

Figure4:ProcessofPhagocytosis

Thecomplementarysystemhasthreemethodsofactivatingacommonpathway,whichhasthreeresultsoreffectors.The threepathwaysthatactivatethecomplementsystemaretheclassical,thealternativeandthelectin.Nomatterthepathway, all3willconvertC3intoC3convertase.ClassicalandLectinPathwaysareactivatedbyantibodies,butinthecaseofthe alternativepathway,C3reactswithnumerousdifferentmoleculeslikewater,FactorBtoformC3bBandeventuallyC3bBb beforeitisconvertedtoC3convertase,wheretheunstablemoleculebreaksdownintoC3aandC3b.C3agoesoffasa messengerproteintorecruitmorephagocyteswhereasthereactiveC3bcanbindtoreceptorsofinfectedcellsallowing phagocytestomoreeasilydigestthem,andC3bcanalsoreactwithC5convertase,C6,C7,C8andseveralC9molecules toformtheComplementmembraneattackcomplex(MAC)whichcausesthecelltolyseanddie.Bydoingthis,thenumber ofhostcellswillbedramaticallyreduced,whichpreventsfurtherproliferationofviralmattertootherregionsofthebody. Yes,thecomplimentarysystemmayalreadyseemunnecessarilycomplicatedwithsomanydifferentproteins,butthrough yearsofevolution,thebodyrealisedthatwithsuchalargenumberofproteins,itallowsformoreamplificationandmore activationsofothercomplements

Buttheinnateimmunesystemisnotalwayscapableofcurbinganinfection,andhencetheadaptiveimmunesystemhas tostepin.Whenthebodyislosingthebattleagainstthevirus,dendriticcellswithantigenspresentedonthemwilltravel acrossthelymphaticsystemtofindTcellsthathasaspecificTcellreceptorthatcanfittheshapeoftheantigen.Tcellsare lymphocytes,buttherearemanydifferenttypesofTcellswithavarietyoffunctionssuchaskillerTcellsandcytotoxicT cells.

IfimmaturekillerTcellsreceptorsbindwiththeMHCClassImoleculesonthesurfaceoftheantigenpresentingcell,they willconverttoKillerTcells(alsoknownascytotoxic/CD8+Tcells).ThesecytotoxicTcellswillgoaroundtotheinfection sitetointeractwiththeantigen-loadedMHCcomplexonthesurfacesofinfectedcells;there,theyreleasecytotoxinswhich wouldinducecelllysisorapoptosis.

Figure6:FormationofMAC

Ontheotherhand,immaturehelperTcells(alsoknownasCD4+Tcells)areactivatedbyMHCClassIImoleculesonthe surfaceandconvertedintohelperTcellsinaprocessknownaspriming.HelperTcellsthentraveltothelymphnodes wheretheyactivatespecificBcellswiththeappropriatepeptideantigen-MHCclassIIcomplexontheBcellssurface.

Bcellsarethefinalimportantadaptiveimmunecellsthatproduceproteinsknownasantibodiesorimmunoglobulins(Ig). EachBcellproducesantibodieswithuniqueantigen-bindingsites,andtheseantibodiesareextremelyimportantin reducingthespreadofviralmatter.

1.

Antibodiesareabletoneutralisefreevirusesbybindingtotheantigenssothattheyareunabletoenterandinfectthe hostcells.

2.

3

Asmostantibodiesmultiple“pincers”,meaningthatitcanbindtodifferentfreeviruses.Hence,theantibodiescan agglutinatetheviruses,reducingtheirabilitytoinfectnearbycellsandmakingiteasierforphagocytestoingestthem.

Antibodiesalsoactivatetwoofthecomplementsystempathways,whichwillleadtomoreMACsandmoreC3a messengerproteinstobeproduced,whichwillstrengthenthecapabilitiesoftheimmunesystem

Finally,theyactivateNaturalKillercellsbybindingtoFcreceptorsonthecells’surface,whichtriggerstheNKcellsto releasemorecytotoxinstokillinfectedcells

Figure7:ActivationofdifferentTcells

Figure8:ActivationofBcellsfromHelperTcells

Withallthisfirepoweragainsttheviruses,yourbodyisalmostdestinedtowinagainstanyviralinfections(withexceptions). Buthowdoesyourbodyensurethatitwon’tgetinfectedagainthenexttimeyoufacetheseviruses?Well,afterthebattleis over,someoftheTcellsandBcellswillturnintomemoryTandBcellsandbestoredbackinthelymphnodesforalong periodofdormancy.Whenthevirusdoesdecidetoreinfectthebody,theimmunesystemwillbeabletorecognisethe antigensquicklyandtriggeraquickerandmoreefficientimmuneresponseasyourmemorycellswillbeabletoproduce theuniqueantibodiesrapidly,whichwillreducethechancesofthevirusproliferatinginmorebodycells.Additionally,there wouldbeahigherlevelofantibodiesofthatdiseasebeingalwayspresentinthebloodstream,sotheimmunesystemwill constantlybeonhighalertfornewinfections.

Figure9:DiagramofanAntibody

Althoughimmunityisbuiltaftertheinitialinfection,italsoseverelyweakenedtheimmunesystem’scapabilityto counterfurtherinfections.Thismakesyourbodymoresusceptibletomorepathogens,whichisnotidealifyou aretryingtobuildupimmunityagainstaparticularlyinfectiousdisease Therefore,scientistshavedeveloped methodstoinduceanimmuneresponsewithoutseverelycompromisingthesystem,andoneofthemostuseful methodsisbyinjectingvaccines.VaccinesoftencontainedweakenedversionsofthevirusorjusttheviralmRNA instructionswhichcanformantigenswhenitinfectsasmallnumberofhostcells.Likeanormalviralinfection,the immunesystemwillbetriggered,leadingtoactivationofTandBcellsandtheproductionofantibodies.Without harmingyourbodyasmuch,memoryTandBcellswillbeproducedtoprotectyoufromfutureinfections.

Inconclusion,theimmunesystemisimpressivelycomplexandsophisticated,andthisarticlealreadyignored many,manyothercellsandchemicalsthatcoordinatetosupportthebodyagainstviralinfections.However,itis stillfascinatingandimportanttoappreciatehowyourbodyprotectsyoufromthemillionsofmicroscopic pathogensthatcouldeasilykillyouwithoutthecoordinationofthemillionsofproteinsandimmunecells.

Bibliography:

[1]https://wwwbritannicacom/science/inflammation

[2]https://wwwncbinlmnihgov/pmc/articles/PMC5472698/#:~:text=Being%20a%20major%20first%20line,killing%20of% 20the%20infected%20cells

[3]https://wwwncbinlmnihgov/books/NBK279396/#:~:text=The%20innate%20immune%20system%20is,the%20%22no nspecific%22%20immune%20system

[4]https://wwwpfizercom/news/articles/how do viruses make us sick#: :text=Once%20a%20virus%20gets%20into,wh ere%20it%20begins%20to%20reproduce

[5]https://wwwncbinlmnihgov/books/NBK8423/#: :text=The%20specific%20immune%20responses%20that,natural%2 0killer%20(NK)%20cells%20and

[6]https://wwwyoutubecom/watch?v=pf1dBxYlxPo

Imagereferences:

Figures:

https://www.britannica.com/summary/virus#/media/1/630244/661381. https://www.nature.com/articles/s41423-021-00650-7/figures/12. https://www.nature.com/articles/nrmicro8173. https://www.nature.com/articles/s41577-023-00921-64.

https://www.frontiersin.org/files/Articles/549867/fimmu-11-01450-HTML/image m/fimmu-11-01450-g001.jpg 5. https://royalsocietypublishing.org/cms/asset/d1e14b45-9fa8-477d-ad6b-1302ddc16280/rstb20160221f01.jpg6. https://commons.wikimedia.org/wiki/File:Antigen presentation.svg 7. https://en.wikipedia.org/wiki/T helper cell#/media/File:Activation of T and B cells.png 8. https://www.news-medical.net/life-sciences/The-Structure-of-an-Antibody.aspx9. https://www.thermofisher.com/hk/en/home/life-science/cell-analysis/cell-analysis-learning-center/immunology-atwork/inflammation-overview.html 10.

MEDICINE

The Impact of Oral Health on Overall Health

By Kingsley Lui

1.0 Introduction

As neglected by many, oral health is a crucial aspect of overall well-being, as it is intricately linked to systemic health and has far-reaching implications for an individual's quality of life The mouth serves as a gateway to the body, and emerging research has revealed profound connections between oral health and various systemic conditions (Kapila, 2021) Beyond its role in maintaining a radiant smile, oral health is vital in the holistic picture of human well-being Therefore, the present research aims to delve into the intricate relationship between oral and systemic health, elucidating how oral health influences various chronic conditions and overall quality of life The subsequent sections will explore the oral-systemic connection, the impact of oral infections and inflammation, the association between oral health and chronic diseases, the relationship with respiratory health, and the implications for an individual's overall quality of life.

2.0UnderstandingtheOral-SystemicConnection

Thereisastronglinkbetweentheoralcavity'shealthandthebody'sgeneralhealth.Thismeansthataperson'soralhealth impactstheiroverallhealth,andviceversa;thestatusoftheirsystemichealthmayimpacttheiroralhealth.Accordingto Kapila(2021),themouthcavityisnotanindependententitybutratheradoorwayintimatelylinkedtotherestofthebody. "Theoralcavityexistsasahighlydynamicmicrobialenvironmentthatharboursmanydistinctsubstrataand microenvironmentshousingdiversemicrobialcommunities"(Kapila,2021,p.14).Kapila(2021)alsoarguedthattheoralsystemicrelationship,whichhasbeenthoroughlyresearched,revealsasignificantdependencybetweenoralhealthand systemicwell-being.However,therelationshipsbetweenoralhealthandvariousillnessesthatextendbeyondthemouth, suchascardiovasculardisease,diabetes,respiratoryinfections,andadversepregnancyoutcomes,arewidely documented(AmericanDentalAssociation(ADA),(2023).

Scientificstudieshaveconfirmedthefunctionoforalhealthasasentinel,givinginformationaboutanindividual'soverall healthstate(ADA,2023;Kapila,2021).Cardiovasculardiseaseisamajorworldwidehealthproblemlinkedtopoordental health(ADA,2023).AccordingtoLeoetal.(2022),inflammationcausedbyoralinfectionsmaycontributetothe developmentofatherosclerosis,adisorderdefinedbytheformationofplaqueinarteries.Itwasalsodiscoveredthatdue topoororalhygiene,dangerousbacteriainthemouthmayenterthecirculation,resultinginbacteremiaandthe multiplicationofgermsonplaquesinsideatheroscleroticcoronaryarteries(Priyamvaraetal 2020) Diabetes,another systemicillness,alsointeractscloselywithpoororalhealth(Kapila,2021) Periodontaldisease,acommondentalissue, maywreakhavoconbloodsugarregulation,aggravatingdiabetes-relatedproblems(ADA,2023) Respiratoryillnesses mayalsoaffectoralhealth Whenoralbacteriaenterthelungs,theymaycontributetothedevelopmentandseverityof respiratoryillnesses(Bezamat,2022) Furthermore,oralhealthmightimpactthewell-beingofexpectingwomenandtheir children AccordingtoKapila(2021),researchshowsacorrelationbetweengumdiseaseandpoorpregnancyoutcomes, underliningthesignificanceoforalhealthinmotherandfoetalwell-being

Thedelicaterelationshipbetweenoralhealthandoverallhealthincludesadiversesetofprocessesormechanisms

Chronicoralinfectionsthatcauseinflammationmayleadtoawidespreadstateofsystemicinflammation,acomponentof manychronicillnesses(Kapila,2021;Bezamat,2022) Immuneresponsesinthemouthcavityreverberatethroughoutthe body,profoundlyimpactingdistantorgansandsystems(Leoetal.,2022).Furthermore,oralbacteriatranslocationintothe circulationprovidestheframeworkforpossiblesystemichealthissues(ADA,2023).Theseresultsshowthe interconnectivityoforalandoverallhealth,emphasisingthevitalnecessityforintegratedhealthcaremethods.

3.0 The Role of Oral Infections and Inflammation

The importance of oral health emerges as a critical aspect within the complicated fabric of health, extending its effect beyond the mouth cavity. The tremendous effect of oral infections, especially periodontal disease, on systemic inflammation is one of these impacts, with far-reaching consequences for chronic illnesses like atherosclerosis and diabetes (ADA, 2023). As a result, the link between oral infections and systemic inflammation is widely established. Periodontal disease, characterised by inflammation of the gums and surrounding tissues, is a significant trigger for producing inflammatory mediators into the circulation (ADA, 2023). This inflammatory cascade extends beyond the mouth cavity, leading to the development and progression of chronic diseases. Atherosclerosis, or the constriction and hardening of arteries, may be exacerbated by inflammation caused by oral infections (Zhu et al. 2022). Furthermore, the inflammatory environment enhances insulin resistance, worsening diabetes-related consequences (Nedosugova et al., 2022)

Oral infections and the body's reaction to them are important to this process. When the equilibrium of microorganisms in the oral cavity is upset, some may become harmful (Kapila, 2023). The immune response to these infections, characterised by the production of cytokines and other immune molecules, feeds systemic inflammation, laying a framework for a negative cycle of health effects (Priyamvara et al., 2020). As a result, these findings demonstrate that solid evidence supports the link between oral infections, inflammation, and systemic health effects. Scientific research has repeatedly shown a link between oral health and oral infections, underlining the deep relationship between oral health and general health (Kapila, 2023; Zhu et al., 2022; Priyamvara et al., 2020). This research convergence emphasises the need to adopt a more comprehensive healthcare strategy that includes oral health as an important component.

4.0 Oral Health and Respiratory Health

The intricate connection between oral and overall health extends to respiratory health, forging a crucial link influencing susceptibility to respiratory infections such as pneumonia and chronic obstructive pulmonary disease (COPD). According to Manger et al. (2017), there is a correlation between oral health and pulmonary conditions, specifically COPD and pneumonia. They hypothesised that sustaining oral hygiene with substances such as chlorhexidine and povidone-iodine could reduce the incidence of pneumonia in patients while brushing one's teeth could reduce the incidence, duration, and fatality of pneumonia in both community and hospital settings. On the other hand, the oral cavity can become a reservoir for pathogenic microorganisms (Kapila, 2021). When aspirated into the airways, these oral bacteria can contribute to the onset or progression of respiratory infections. Research illuminates the potential for oral microorganisms to cause or exacerbate respiratory infections, disclosing the systemic implications of compromised oral health (ADA, 2023). The presence of periodontal disease and the accompanying inflammatory response fosters the spread of pathogenic bacteria throughout the body, including the respiratory system (Priyamvara et al., 2020).

However, this association also opens the door to promising interventions. It was reported that interventions designed to improve oral health have been shown to reduce the risk of respiratory infections. Medical professionals can reduce the incidence of respiratory disorders by focusing on eliminating oral pathogens and inflammation (Manger et al. 2017).

5.0 Oral Health and Overall Quality of Life

Oral health is crucial in determining a person's overall quality of life beyond its influence on physical health. Taking everything into account, it is almost certain that poor oral health creates problems that extend well beyond the mouth, as well as decreasing or diminishing the quality of life Oral discomfort and pain can substantially restrict daily activities, including eating, speaking, and even basic duties like smiling (Block et al , 2022) Such restrictions diminish a person's capacity to engage with the world completely, diminishing their sense of normalcy and happiness

Nonetheless, the consequences extend beyond the physical domain The psychological and social consequences of poor oral health are significant Individuals with oral issues frequently struggle with low selfesteem and confidence due to concerns regarding their appearance and breath odour (Block et al , 2022; Australian and New Zealand Mental Health Association, 2023) On the other hand, it was found that social interactions may be impeded, leading to feelings of isolation and even despair The stigma associated with oral health issues exacerbates these difficulties, increasing the psychological toll (Baiju et al 2017)

In contrast, enhanced oral health significantly impacts an individual's quality of life. Individuals regain the ability to eat, speak, and smile with confidence when pain and distress are eliminated (Kapila, 2021). This restoration of functional and aesthetically pleasing features enhances physical comfort and benefits mental health. The Australian and New Zealand Mental Health Association revealed that the positive effect on selfesteem could promote a more optimistic outlook on life, reinforcing the link between oral health and emotional health. The ripple effects also extend to social interactions. Enhanced oral health facilitates easier and more pleasurable social interactions, strengthening relationships and fostering a sense of belonging. This contributes to overall contentment and life satisfaction.

6.0 Conclusion

The investigation of the interrelation between oral health and general well-being reveals that the disregard for oral health might result in significant and wide-ranging ramifications. The existing body of literature presents substantial evidence supporting the interconnectedness between oral health and chronic illnesses, emphasising the imperative for integrating healthcare services. The known correlations between inadequate oral hygiene and chronic conditions such as diabetes, heart disease, and respiratory infections underscore the need for a holistic healthcare approach. The consequences of this understanding have substantial issues for public health policies and practices, necessitating a shift that recognises the role of oral health in overall well-being.

Given the facts above, issuing a call to action is imperative. Individuals must prioritise their oral health, acknowledging its significance in preserving overall well-being. Implementing integrated healthcare strategies incorporating dental care can mitigate the impact of chronic illnesses and improve overall wellbeing. Simple practices such as regular dental checkups, brushing and flossing, and a healthy diet are key to preventing the development of oral health problems. According to the American Dental Association, brushing twice daily with fluoride toothpaste and flossing daily can help prevent tooth decay and gum disease. Through adopting proactive oral health practices, individuals can assume responsibility for their overall wellbeing, thereby facilitating the cultivation of better lifestyles.

7.0 Biblography

[1]American Dental Association (ADA) (2023) Oral-systemic health https://www ada org/en/resources/research/science-and-research-institute/oral-health-topics/oral-systemichealth

[2]Australian & New Zealand Mental Health Association (April 6, 2023) How Oral Problems Affect Your SelfEsteem https://anzmh asn au/blog/how-oral-problems-affect-your-self-esteem

[3]Baiju, R M , Peter, E , Varghese, N O , & Sivaram, R (2017) Oral Health and Quality of Life: Current Concepts Journal of clinical and diagnostic research: JCDR, 11(6), ZE21–ZE26 https://doi org/10 7860/JCDR/2017/25866 10110

[4]Bezamat M. (2022). An updated review on the link between oral infections and atherosclerotic cardiovascular disease with a focus on phenomics. Frontiers in physiology, 13, 1101398. https://doi.org/10.3389/fphys.2022.1101398

[5]Block, C., König, H. H., & Hajek, A. (2022). Oral health and quality of life: findings from the Survey of Health, Ageing and Retirement in Europe. BMC Oral Health, 22(1), 606. https://doi.org/10.1186/s12903-022-02599-z

[6]Centres for Disease Control & Prevention (CDC). (April 6, 2022). Oral health conditions. https://www.cdc.gov/oralhealth/conditions/index.html

[7]Guo, D., Shi, Z., Luo, Y., Ding, R., & He, P. (2023). Association between oral health behaviour and chronic diseases among middle-aged and older adults in Beijing, China. BMC oral health, 23(1), 97. https://doi.org/10.1186/s12903-023-02764-y

[8]Kapila Y. L. (2021). Oral health's inextricable connection to systemic health: Special populations bring to bear multimodal relationships and factors connecting periodontal disease to systemic diseases and conditions. Periodontology 2000, 87(1), 11–16. https://doi.org/10.1111/prd.12398

[9]Leão, T. S. S., Tomasi, G. H., Conzatti, L. P., Marrone, L. C. P., Reynolds, M. A., & Gomes, M. S. (2022). Oral Inflammatory Burden and Carotid Atherosclerosis Among Stroke Patients. Journal of Endodontics, 48(5), 597–605. https://doi.org/10.1016/j.joen.2022.01.019

[10]Manger, D., Walshaw, M., Fitzgerald, R., Doughty, J., Wanyonyi, K. L., White, S., & Gallagher, J. E. (2017). Evidence summary: the relationship between oral health and pulmonary disease. British dental journal, 222(7), 527-533. https://www.nature.com/articles/sj.bdj.2017.315

[11]Nedosugova, L. V., Markina, Y. V., Bochkareva, L. A., Kuzina, I. A., Petunina, N. A., Yudina, I. Y., & Kirichenko, T. V. (2022). Inflammatory Mechanisms of Diabetes and Its Vascular Complications. Biomedicines, 10(5), 1168. https://doi.org/10.3390/biomedicines10051168

[12]Priyamvara, A., Dey, A. K., Bandyopadhyay, D., Katikineni, V., Zaghlol, R., Basyal, B., Barssoum, K., Amarin, R., Bhatt, D L , & Lavie, C J (2020) Periodontal Inflammation and the Risk of Cardiovascular Disease Current atherosclerosis reports, 22(7), 28 https://doi org/10 1007/s11883-020-00848-6

[13]Zhu, X , Huang, H , & Zhao, L (2022) PAMPs and DAMPs as the Bridge Between Periodontitis and Atherosclerosis: The Potential Therapeutic Targets Frontiers in cell and developmental biology, 10, 856118 https://doi org/10 3389/fcell 2022 856118 Medicine-37

PRedefining rosthetics:

Evaluating 3D-Printing in Revolutionising Medical Intervention

By Caitlyn Tang

1.0 Introduction

Picture this: a patient cured of an aggressive form of face cancer but left with an apple-sized hole in their cheek , a haunting reminder of the battle they’ve endured Yet amid their despair where traditional medicine and ill-fitted prosthesis fell short, a glimmer of hope emerges in the form of a ground-breaking solution: the ability to sculpt a precise 3D-printed prosthetic customised precisely to their anatomy, ensuring optimal fit and function This dream is now a reality, made possible simply by smartphones and a low-cost 3D-printer

In the realm of modern medicine, precision is paramount The advent of 3D-printing technology has heralded a new era of healthcare, revolutionising disciplines such as dentistry, orthopaedics, and oncology

This article evaluates the efficacy of 3D-printing in enhancing prosthetics and improving patient outcomes, while confronting the ethical considerations, limitations and challenges posed by it.

2.0Background-ProstheticsThroughtheAges

3D-Printingwasinventedin1981byDrHideoKodamathroughmanyattemptstomodifytheprototypeofanoldinkjet printer.Theprocessoriginatesfromstereolithography,whichusesaUVlasertocurelayersofphotopolymerresin, graduallyformingthedesiredshapeofthefinalproduct.ThiswasSelectiveLaserSintering(SLS),where,asthename implies,plastic,metal,glassorceramicpowderisselectivelyfusedviaheatingbylaserenergy ReferringtoFigure2,a powderisspreadevenlyoverthesurfaceofabuildplatform,andascannerfocusesitslaseruniformlythroughouttillthe wholelayeriscomplete Anewlayerofpowderisdepositedontopandthecyclerepeats(Charooetal,2020)

Inmedicine,thistypicallyincludestheadditionoftomographyorX-rayimagesconvertedforuseintheSLSsystem,with computer-aideddesign(CAD).(Dodziuk,2016)Inaddition,whilstthetypicalmaterialslikeplastic,glass,metalandsand areused,softmaterialssuchasbiomaterials,livingcells,biopolymers,andsiliconescanbeutilisedfortissueengineering knownasbioprinting(Maneroetal.,2019).

3.0 Comparison of 3D-Printing of Prosthetics to Traditional Manufacturing

The aforementioned applications of 3D-printing in Healthcare are vast, ranging from customised prosthetics, implants, tissue, organs, surgical instruments, pharmaceuticals, drug delivery devices, and other medical devices (Dodziuk, 2016).

3.1 Precision

Theautomatednatureof3D-Printingundoubtedlyresultsinhigherprecisioncomparedtothetraditionalmanufacturing methods.Examplesofthiscanbeseeninporousprosthetics,suchasboneimplants.Moreover,mostprostheticsrequire componentsthatcanmovetogetherseamlessly,-andonly3Dprintingcaninterpretandmimicalljointmovementsina singlerunofproduction.Incontrast,traditionalmanufacturinginvolvessubtractiveprocesseslikecuttingordrilling materialsintotherightshapewhereas3D-printingisanadditivetechnology.

ReferringtoFigure1,astudyconductedbyIbrahimetalinvestigatedthedimensionalaccuracyof3D-printed mandibularanatomyreplicasusinghelicalCTscans Theresultsshowedatotalmeandimensionalerrorof179%,for SLS(selectivelasersintering),implyingthehighaccuracyofSLStechnologyinreproducinganatomicaldetails

3.2 Time and Cost of Production Process

Mostprostheticdevicesarenotperfectlysuitedforrecipients,asitismorecost-effectivetocreatestandardisedsizes suitablefortheaveragepatient.Theproductionoftraditionalprosthesistakesweeksifnotmonthsandsonotonlyisit time-consuming,butalsocostly,botharefactorsaffectingapatient’sdecisiontochoosetraditionalprostheses.The Global3D-PrintedProstheticsMarketReportof2022foundthat3D-printedprostheticscancostaslowas50USD,whilst theirtraditionalcounterpartscancostmuchmore,rangingfrom$1,500to$8000.Furthermore,studiessuchasBallard etal.haveshownthattraditionalprostheticslastamuchshortertimeduetoahigherlikelihoodofwearandtearthan3Dprintedprosthetics.

Instarkcontrast,3D-printingseemstohavemuchtoofferintermsofaffordabilityandproductiontime.Thesecustom devicesarenowmuchmorereadilyavailable,quicklyproduced(typicallywithinaday)andpreciselytailoredto recipients.

3.3 Patient Outcomes

Equallyimportantaspectstoconsiderinprostheticcustomisationarepatientsatisfactionandoutcomes Traditionally manufacturedlimbshavebeenseentodomoreharmthangood,causingrecipientdiscomfortthataddstothestressof patients’lives-fromanecdotalevidence,reducingqualityoflife Thisisoftenseeninmandibularcancers,whichrequire significantboneandsofttissuereconstructionaftertumourresection-traditionalsizingissimplynotanoptioninfacial reconstruction,foraesthetic,comfortaswellasdurabilityreasons(Mitsourasetal,2015) Astoucheduponinthe introduction,54-year-oldpatientCarlitoConceiçaoisthefirstpersontohavereceiveda3D-printedfaceprosthesismade withasmartphoneafteranuppermaxillarycarcinomaleftaholeinhischeek.Hestatedthathavinglosthisrighteye socketandpartofhisnose,hisfirsttraditionalprosthesiswas‘fragile,[of]poorqualityandkeptfallingoffbecauseitwas heldonbyglue’.Heexpressedalossofconfidenceandfearofjudgementfromothersinpublic,whichcausedhimto descendintoastateofdepressionduetohisinabilitytowork.

Thispainandstresshasbeengreatlyalleviatedthroughthequickandeasycomfortof3D-printedprosthesis,aidedwith theabilitytocustomisecolourandstyle InthecaseofConceiçao,thelow-cost,never-seen-beforeprocedurenamedPlus IDusedthefreeapp,Autodesk123DCatch,whichturnsphotosinto3Dmodels.Theprocessinvolvedtaking15photosof thetraumaareafProstheticsareneededformanydifferentconditionsincludingamputationsandcongenitalorgan malformationslikeagenesisandhypoplasia.ThoughtheoriginsofprosthesisdatesbacktoancientEgyptianandRoman times,anotableindividualwhospearheadeditsdevelopmentisJohnHanger.Hanger,anengineerandinventor,hadhis legamputatedduringtheCivilWarafteraseriousinjury(NIHMedlinePlus,2023).Refusingtobelimitedbyhismissing limb,hedevelopedanartificiallimbusingoakbarrelstaves,rubberbumpers,andnailsboastingthecapabilitytoflexat boththekneeandanklejoints.Namingthisthe‘HangerLimb’,itgainedtractionasahighlyregardedsolutiontothemany maimedConfederatesoldiersofhistime.Sincethenadvancementssuchascables,gearsandspringshaveimproved prostheticlimbs,providinggreatermobilitytorotate,pickuputensils,andevenplaythepiano.

Inthe21stcentury,prostheticlimbshavebecomemuchmoredurableandlightweight.Theyareusuallymadeofplastic, aluminium,orsilicone,andcanevenbecustomisedtohavetattoosforaestheticpurposes.Bioengineeringtechnology hasmadeitpossibletouseAIandimplantedelectrodestofacilitatecommunicationbetweenapatient'slimbs,muscles andthebrain,creatingmorenaturalmovements.Whilstreplacinglimbsisahugepartofprosthetics,moderndayrom differentanglesandconvertingthemintoavirtualmodelofthepatient’sface,whichtook20hours.Thehealthysideofhis facewasthenmirroredtocreateatemplateofwhattheprostheticshouldlooklike.Oncethesiliconprosthesiswasmade, volunteerclinicalartistsaddedskincolours,textureandrealisticwrinklestomaketheprostheticlookevenmorenatural. Insteadofbeingattachedbyglue,thisnewprosthesiswasfittedwithmagnetsthatlockedontothreetitaniumscrews embeddedunderCarlito'seyebrow,ensuringthatitwouldstayanchoredatthatpointalleviatingpatients’fearsofitfalling offinpublic.Itisevidentthat3D-printingprovidesbenefitsintheaspectofrapidcustomisationofcost-effective prototypingandprosthesisproduction.

Theuseofdentalimplantshasbecomeawidelyacceptedmethodforrestoringmissingteeth Theseimplantsare typicallymadefrombiocompatiblematerialssuchastitanium,asitisshowntohaveexcellentbiocompatibilityand osseointegrationproperties.TitaniumalloyssuchasTiZr(titanium-zirconium)andTi6Al4V(titanium-6aluminum4vanadium)havebettermechanicalfeaturesduetotheirbetterdurabilityandintegration.Surfacemodificationslike microroughnessandacid-etchinghavebeenshowntoenhancetheinteractionbetweentheimplantandthe surroundingtissues,promotingfasterhealingandbetterintegration(Ashtianietal.).Additionally,theuseofantimicrobial coatingsontheimplantsurfacecanhelppreventbacterialcolonisationandsubsequentinfections,whicharecommon causesofimplantfailure.

Inrecentyears,therehasbeenagrowinginterestinthedevelopmentofbiomaterialsfordentalpulpregeneration.These biomaterials,suchaschitosanandpolyhydroxyalkanoates,havebeenshowntopromotetheregenerationofdentalpulp tissueandenhancethehealingprocess(Ashtianietal).Theycanbeusedasscaffoldsfortissueengineeringorascarriers forgrowthfactorsandotherbioactivemolecules.Furthermore,theuseofbioactivematerialslikebioactiveglassand calciumphosphate-basedmaterialscanstimulateboneregenerationandenhanceosseointegration,leadingtobetter long-termoutcomesfordentalimplants.

3D-bioprintingholdsgreatpromiseforaddressingtheshortageoforgandonorsbymanufacturinghumantissueusing 3D-printingtechnology.Whiletheultimategoalistocreatefullyfunctionalorgansfortransplantation,current achievementsaremoremodest,focusingonapplicationssuchaslab-on-the-chipmodelsforresearch,drugdiscovery, andtoxicology(Dodziuk,2016).

Keyadvancementsincludethedevelopmentof‘thawanduse’humanmesenchymalstemcellbioinkbycompanieslike CellinkandRoosterBio,aswellastheuseofself-healingbioglassforcartilagereplacement.Researchershavesuccessfully 3D-bioprintedflattissues(suchasskin),tubularstructures(suchasthetrachea,urethra,andbladder),andcomplexsolid organs(suchastheliver).SomeChineseresearchershavereportedusing3D-bioprintingtocreatetissuesofthekidney, ears,andlivers,althoughthesetissuesmaynotbereadyforimplantation.

5.0 Challenges, Limitations and Ethical Considerations

Oneofthechallengesof3D-printedprostheticsisthedurabilityofthedevice.Dueto3D-printingconsistingmainlyofthin layersofhotplasticorsiliconlaidontopofeachother,theycanbepronetobreakingeasily.Astudyofthedurabilityoflowcost,3D-printedtranstibialprostheticsockets,whichconnecttheresiduallimbtotheprosthetic,conductedtwo mechanicaltestsThestatictestandthecyclictestaimstosimulatewalkingandtohelpmeasurethemaximumloadthat couldbeperformedontheprosthesis.Resultsincludedtensilestrengthandtensileelongationatthebreakingpoint.The studyalsocomparedthedurabilityofmaterialsusedtomake3D-printedprosthetics,revealingthatsometraditionally manufacturedprostheticsindeedweremoredurableinthelong-term.Theseconflictingevidencefromvariousstudies madeitunclearwhether3D-printedprostheticscanadequatelyreplacetraditionalones.

Theethicalconcernsregardingthereimbursementprocessforprostheticsareaffectedbyamultitudeofreasons.Oneof theprimaryconcernsistheissueofequityandaccess.Thecurrentsystemmaycauseunequalaccesstoprostheticsfor patientswithdifferentclinicalneeds,potentiallyleadingtodisparitiesinhealthoutcomesbasedonsocioeconomicstatus orotherfactors.Thelackofqualitycareandaccessisseeninmanycountries,fromtheUS(AMAJournalofEthics,2015), Canada(PetlockandDiMario,2021)andGermany(Baumannetal.,2020)toRwanda(Ngarambeetal.,2022).Thisis particularlyconcerninginacountrylikeGermany,whichpridesitselfonitscommitmenttosocialwelfareandinclusivityas seenincriteriarecommendedbytheGermanCentralEthicsCommissiononmedicine(ZentraleEthikkommission,ZEKO), andtheSocialCodeBook(SGB,Sozialgesetzbuch).

Affordabilityisasignificantconcerninthecontextof3D-prostheticreimbursement Thecostofprostheticscancreatea substantialfinancialburdenforindividualsandfamilies,particularlyiftheyarenotfullyreimbursedbyinsurance ProstheticreimbursementposesagreatissueinGermany,anissuehighlightedinastudybyBaumannetal,which notesthat37%ofprosthesiswearersinGermanywerenotfullyreimbursedfortheirexpenses,and48%ofnon-wearers consideredcostaninfluentialfactorintheirdecisionnottowearprostheses Financialbarrierscertainlylimitaccessto prosthetics,notjustduetoreimbursement,butbecauseofhighcostsoralackofinsurancecoveragethatprevent patientsfromaffordingtheprostheticstheyneed.Thisisparticularlyconcerninggiventheimportanceofearlyfittingfor sustainedprosthesiswear,aswellassignificantlyimpactinganindividual'sabilitytoparticipateinsocialevents,aswell astheiroverallqualityoflife.

InlowerincomecountrieslikeRwanda,theissueofavailabilityandaccesstoprostheticsismorepressing.Astudy conductedbyNgarambeetalrevealedthatof3026participants,60.3%ofmaleamputeesdidnotevenhaveaccesstoa prosthesis.Ofthosewhodidhaveprostheticdevices,62.4%weredamagedandhadnotbeenrepaired.63.7%ofthese amputeesdidnothaveasourceofincomeandsolackedthefinancialandphysicalmobilitytoseekaidfortheir prosthetics.Itisevidentthatmoreworkmustbedonetounifyqualityaccesstoprostheticsworldwide,forexample throughgovernmentcooperationwithNGOsandstakeholderstomakeprostheticrehabilitationmoreaffordablefor thoselackingthefunds.

IntheUnitedStates,theregulationoforganmatchinghasproveninadequateinaddressingthehighdemandfororgans duetotransplantation.Organprintingtechnologyhasemergedasapotentialsolutiontothisimbalancebyenablingthe productionofpatient-specificorgans.However,thepracticalimplementationoforganprintingiscontingentupon regulatoryframeworks.

Printedorgansareconsideredmultifunctionalcombinationproducts,fallingbetweenthebiologicsanddevicessectors intheFDA.Inresponse,theFDAissued‘TechnicalConsiderationsforAdditiveManufacturedDevices’in2o16as guidanceforevaluationof3D-printeddevices(CenterforDevicesandRadiologicalHealth,2019).However,3D-printing technologyisnotadvancedenoughfortheFDAtofullyincorporateitintomainstreammedicalpractice.Currently,the focusisonevaluatingtheefficiencyandsafetyof3D-printerstostandardisethetechnologyforfuturetailoredtreatments .Ifwelooktoothercountries,onlyJapanandSouthKoreahavesuccessfullydevelopedguidelinesformedicaldevice regulationthatcouldbeappliedto3D-bioprinting(Wolinsky,2014) Additionally,intellectualpropertyandownership issuessurrounding3D-bioprintingraiseconcernsaboutqualitycontrol,piracy,andunauthorisedusageontheblack market Thesefactorscontributetothecomplexityofregulating3D-bioprintingtechnology,illustratingtheneedfor comprehensiveregulatoryframeworkstoensureitssafeandeffectiveimplementation

Fromanethicalperspective,cellsourcesin3D-printedorgansandprostheticsarecausingconsiderabledisquiet For example,artificiallyproducedorganscanbeusedinillegaltraffickingasanalternativetoharvesting Moreover,despite organ-printingbeingsignificantlycheaperthantraditionalsurgicaltransplantation,thereisgreatscepticismsurrounding howwell-receiveditwillbe,duetoclasheswithcultural,social,andreligiousdifferences InastudybySabrietal, researchersinvestigated3Dorgan-printingfromtheperspectiveofIslamictraditionandlaw Theydiscussedhowthe alterationofGod’sCreationwentagainstMuslimorIslamicprinciples,quotingchapter4verse119oftheQuran‘[Satan said]AndIwillmisleadthem,andIwillcreateinthemfalsedesires,Iwillcommandthemtoslittheearsofcattle,andIwill commandthemtochangetheGod'screation.’Whilstthiswentagainsttheirreligiousprinciples,theresearchers discussedtheargumentsforandagainst3Dorgan-printing,weighingtheclearbenefitsofsavingalifetoviolationof Islamiclaw,inwhichtheQuranisheavilyreferenced.(Sabrietal.,2022)

Anothermajorconcernof3Dprintingistheissueofconfidentialityandprivacyespeciallyintheaforementioned bioprinting.Asitinvolvesprocessinglargeamountsofhumandata,thisposesasecurityriskindonorconfidentialityin regardstohowthegeneticinformationisstoredandused.(Kirillovaetal.,2020)Researchintothepossibilitymeans thereisahigherlikelihoodofgeneticdatabeingleakedorusedformaliciouspurposes-soinformeddonorconsentis incrediblyimportant.However,thisopensaseparatecanofwormswheresomedonorsareintheICUoremergency medicalsituations.Thisdiminishestheirabilitytomakeaninformeddecision;itisvitalthatclear-cutrulesandregulations areimplementedtoavoidmalpractice.

Asbioprintingisstillarelativelynewfield,insufficientclinicaltrialshavebeenconducted,andespeciallynotonhumans. Itisunclearwhetherhumanbodieswillrejectlab-grownorgans,andintheexampleof3Dbioprintedovaries,itisunclear whethermanipulationstogeneticsandtheresultanteggcellswillaffectoffspring.

6.0 Conclusion

Themedicalfieldhasseensignificantadvancementsinrecentyears,rangingfrom3D-printedprostheticstobioprinting organs However,thereisstillampleroomforfurtherimprovements Futurestudiesmustbecarriedouttoexplorethe long-termhealthconcernsandlongevityof3D-printedhealthcaredevices.Theseadvancementshavethepotentialto revolutionisethefieldoforganprintingandaddresstheorgantransplantshortage.

3D-printinginmedicineisstillarelativelynewfieldofresearch-asthiscontinuestoprogress,itisexpectedthatthese developmentswillcontributetomorerealisticandeffectivesurgicalsimulations,ultimatelybenefitingpatientcareand outcomes.Despitetheethicalandregulatoryhurdlesassociatedwith3Dprinting,itisevidentthatithasalreadyhadand willcontinuetohaveatransformativeimpactonhealthcaretechnologyandimplantablemedicaldevices.

7.0 Bibliography

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PHYSICS

By Jeffrey Ling

An Insight Into Quantum Entanglement

1.0 Introduction

Imagine a rock. Now imagine a hammer. If we use the hammer to hit the rock, it will turn into pebbles, and if we hit the pebbles enough times, it might even become dust But is this the furthest we can go? Well, if we could split the dust somehow, we would get the atoms that made up the rock, and if we split the atoms, we would find protons, neutrons, and electrons Finally, our last step is to split the protons and neutrons into something even smaller - quarks. To give you a point of comparison, quarks are 10-16 centimetres, and this realm of the super super small (called Particle Physics) dictates how our universe runs and describes every interaction. However, this realm seems to follow complete different and strange rules of physics, and as such has stumped the greatest scientists of the past century. One of these strange interactions is quantum entanglement, or as Einstein calls it, ‘Spooky Action at a Distance’.

2.0Background

TheStandardModelofParticlePhysicsstatesthateverything inouruniverseismadeupof‘ElementaryParticles’,for examplequarksandelectrons.Alltheseelementaryparticles havepropertieslikemassandcharge,buttheonethatis importantforquantumentanglementiscalled‘spin’.Spincan bethoughtofasameasureofangularmomentum,however unlikemassandcharge,itdoesnothaveanumericalvalue andcanonlyhave‘up’or‘down’,andthisvaluechanges dependingontheorientationthatyoumeasureit.Whentwo particlesare‘entangled’,theirspinvaluesareconnectedas suchthatwhenmeasuredfromthesameorientation,their valuesmustbeopposite.Forexample,ifparticlesAandBare entangled,andparticleAismeasured,inadirection,tohave spinup,thenweknowthatparticleBwill,forthatsame direction,havespindown.Weknowthatthisneedstobetrue becauseangularmomentum,likeenergyormomentum, mustbeconserved

2.1Bohr’sCopenhagenInterpretation

Inthe1900s,oneofthetwomaincampsofQuantumTheorysupportedthatofanon-objectivereality,meaningthatthe quantumuniverseonlyhadanyrealmeaningwhenmeasured,andwhennotmeasured,quantumsystemsexistedasa superpositionofallstatesdescribedbytheirquantumwavefunction,whichcanonlygiveaprobabilisticchanceofthe stateoftheobject.Toputthisconceptanalogously,it’stosaythatwhenwelookaway(stopmeasuring)fromanobject, theobjectisinasuperpositionofallstates,somemixturewithallpropertiesthatcanonlybedescribedthroughafunction thatformulatesaprobabilityofwhatitcouldbeandallowsustomakepredictions.AnotherideawithintheCopenhagen Interpretation,Bohr’scomplementarityconcept,suggeststhattheactofmeasuringaparticlecausestheprobabilistic wavefunctiontocollapseandsetsarealvalueontotheparticle.Thisisakintoputtinglightthroughapolarisingfilter whichdeterminesthedirectionofoscillationwhenusedtomeasurelight,astheactofmeasuringalsodeterminesthe alignmentofspin[1].

2.2TheEPRParadox

ThesecondcampofQuantumTheoryrejectedthiskindof‘peek-a-boo’universewhereparticlesonlyhadvaluewhen measured,andinsteadbelievedinanobjectivereality.MostfamouslyheadedbyEinstein,hewastroubledbythefactthat measuringaparticlecouldinstantaneouslyaffectthestateofaparticlelightyearsawayasitviolatedthelawsofrealism.In hisfamousEPRpaper,publishedalongwithphysicistsBorisPodolskyandNathanRosen,theydetailathought experimentthatbasicallysaidthatiftheCopenhagenInterpretationwascorrect,itwouldviolate‘locality’andbyextension Einstein’s‘relativity’-theconceptthatanyparticlecouldonlyaffectitsimmediatesurroundings,andthatthechainof causeandeffectcannotpropagatefasterthanthespeedoflight–soinformationcannotpossiblygetfromParticleAto ParticleBfasterthanthespeedoflight

Therefore,EPRconcludedthatentanglementcouldnotbesometypeofcauseandeffect-theremustbesomeotherlocal hiddenvariablesinherentintheparticlesthatdeterminedthedirectionofspinfromanyanglefromwhentheyarecreated. Thus,thisexplainswhyweseeacorrelationwhenmeasuringtheparticles,whilstthereneednotbeinformationtravelling betweenthetwofasterthanthespeedoflight[2,3]

Figure2–Tableanddiagramillustratingprobabilitiesofmentionedtest casesthatonewouldexpecttoseewithEinstein’s‘HiddenVariables’ theory

2.3Bell’sInequalityandtheCHSHExperiment

Atthetimethisdebateseemedmorephilosophical,untilin1964physicistJohnBelldevisedaninequalitytoproveifeither sidewasright.Thebasisoftheexperimenthas2hypotheticalcharactersAliceandBob,whoeachreceiveoneparticleof anentangledpair.Theyeachmeasurethespinoftheparticlerandomlyinoneofthreedirections(A0,A1,A2;B0,B1,B2), butAlice’sdecisiondoesnotaffectBob’sdecisionandviceversa(byassumingthiswepreservelocality).Furthermore,the particles’otherphysicalpropertiesexistindependentlyofbeingmeasured(sothatrealismisalsoassumed).Theoutcomes ofAliceandBob’smeasurementscanbe+1forspinup,and-1forspindown.Bydeterminingthepercentageinwhich theirmeasurementsarethesame,wecanconcludewhetherEinsteinorBohrwascorrect.AssumingthatEinsteinwas right,themeasuredspinoftheparticleispre-determinedinthethreedirectionsandtheonlycorrelationbetweenparticles isthattheyhaveoppositespinwhenmeasuredinthesamedirection.Letusconsidertwocases:A0=+1,A1=+1andA2= +1,B0=-1,B1=-2,B2=-3;orsimplydenotedasA(1,1,1)andB(-1,-1-1). ThesecondcaseisA(1,-1,1)andB(-1,1,-1).In thefirstcase,AliceandBobwillmeasureoppositespins100%ofthetimeandinthesecondcase,AliceandBobwill measureoppositespins5outof9times(55.5%ofthetime).(*Othercasesaremathematicallyequivalentsowecanfocus onthesetwocases;RefertoFigure2forclarification.)Therefore,ifweassumethatEinsteinwascorrect,wecanexpectto getdifferentresultsbetween55.5%to100%ofthetime[4].

Thisinequalitywastestedin1969byateamconsistingofJohnClauser,MichaelHorne,AbnerShimony,andRichardHolt byfiringabeamofphotonsataBBOcrystalwhichcancausesome(≈6ineverymillion)photonsto‘downconvert’into twoentangledphotonswithhalftheenergy Theentangledpaireachpassthroughapolariseranddetectorthenthedata issenttoanalyse Itseemsrelevanttonotethatthisexperimentdetects±1byseeingwhetherthephotonpassesthrough thefilter Whattheteamfoundaftermanyrepetitionswasthattheresultswereonlydifferent50%ofthetime,which showedthatEinsteinwaswrong IfweinsteadconsiderthatA0=1,theresultofanysubsequentmeasurementdepends ontheanglebetweenA0andthenewmeasuringdirection-ifthenewmeasurementdirectionismorealignedwithA0, thenitismorelikelytoreturn1aswell,theprobabilityisfoundtobecosine(θangle/2)squared.

Figure4–Graphicalrepresentationofexpectedresultsthrough

3.0ApplicationsofQuantumEntanglement

InthecasesofA1and2,itwouldbe120˚fromA0so cosine(120/2)2=1/4.SogiventhatA0=1,weknow thatB0=-1andB1andB2havea1/4tobe-1aswellthereisa1/3chanceofchoosingB0and2/3chance ofchoosingB1/2andafurther1/4chanceforthe measurementtobeoppositeofA0 Tosummarise giventhatA0=1,thereisa1/3+(2/3*1/4)=1/2 chancethatthemeasurementsfromdetectorsAandB aredifferent-exactlywhatClauser’sexperimentfound Anotherwaytounderstandthisistolookatit graphically Bycomparingcorrelationtodifferencein anglebetweendetectors,wecanseeadifference whenassuminglocalhiddenvariablesornot-classical meanswhatEinsteinwouldhaveexpectedtosee Similarly,bylookingattheresultsfromClauser's experiment,wefindthatitfitsthequantumcosine curvebetter.RefertoFigure4formoredetail.

QuantumComputingisoneofthecomplexwaysinwhichweharnessthepowerofquantummechanics.Whileclassical computersstoredatausingbitsthatrepresent0and1,quantumcomputersstoredatausingqubits,whosestatesare describedasalinearcombinationof0sand1sasitisinastateofsuperposition,analternativewaytodescribethisisthat thequbithassomeamplitudeof0sandsomeamplitudesof1,whereamplitudeistheprobabilisticwavefunctionthatitis 0or1;quantumalgorithmsmanipulateamplitudesinawaysuchthatthereisahigherprobabilitytoreturnthecorrect answer.Thispropertyallowsittorepresentmanydifferentvaluesinparallel;Forexample,given10qubits,youcouldstore 210valuesinparallel.Hereitbecomesclearwhythereisaneedforquantumcomputing-becauseaswescaleupin qubits,itcanrepresentexponentiallymorevaluesandsoittakesmoreandmorebitstokeepup.Asidefromsuperposition, quantumcomputersalsouseentanglementtotheiradvantage.Aspreviouslyproven,weknowthatthereiscorrelation betweenanentangledpairofparticles;insupercomputersthedataisstoredwithinthecorrelationsbetweenentangled partsofaquantumsystem.Ahelpfulanalogyisabookinwhichthereis‘gibberish’oneachpagewhenlookedat individuallybecausetherealinformationisinthecorrelationamongthem,sowemustlookatallpagescollectively. QuantumentanglementisalsousedwithinquantumalgorithmssuchasGrover’sAlgorithmfordatabasesearchesand QuantumErrorCorrection,whichisusedtocheckforerrorduringquantumcalculations.Althoughthisisanexciting prospectforthefutureofcomputing,itisunlikelythatthiswillreplaceclassicalcomputersorsupercomputersbecause storingdataonitisinconvenientasitismorefragileandpronetoerror.Furthermore,itcanbeslowerthanclassical computersinsomerespectsduetoitsprobabilisticnaturewhichrequireserrorcheckingalgorithmssuchasQuantum ErrorCorrectionasmentionedabove[5]

4.0Conclusion

Quantumentanglementstandsasoneofthemostprofoundandintriguingphenomenaintherealmofquantumphysics andmanyphysicistsbelieveinitsprospectwithitspotentialapplicationsinquantumcomputing,cybersecurity, simulations,etc.Evenafterdecadesofresearchandgroundbreakingexperiments,wearestillyettohavefullyunderstood thisconcept,itiscertainthatcontinuingtoexplorequantumentanglementwillhelpshapeourunderstandingofthe fundamentalnatureoftheuniverse.

5.0Bibliography

[1]Jones,AndrewZimmerman.“WhatIstheCopenhagenInterpretation?”ThoughtCo,ThoughtCo,31Dec.2013, https://www.thoughtco.com/copenhagen-interpretation-of-quantum-mechanics-2699346.

[2]Jones,AndrewZimmerman.“EPRParadoxinPhysics-DefinitionandExplanation.”ThoughtCo,ThoughtCo,23Mar. 2012,https://www.thoughtco.com/epr-paradox-in-physics-2699186.

[3]QuantumEntanglementandtheGreatBohr-EinsteinDebate|SpaceTime|PBSDigitalStudios,YouTube,uploaded byPBSSpaceTime,22Sept.2016,https://www.youtube.com/watch?v=tafGL02EUOA.

[4]QuantumEntanglement&SpookyActionataDistance,YouTube,uploadedbyVeritasium,13Jan 2015, https://wwwyoutubecom/watch?v=ZuvK-od647c

[5]QuantumComputers,ExplainedWithQuantumPhysics,YouTube,uploadedbyQuantaMagazine,8Jun 2021, https://wwwyoutubecom/watch?v=jHoEjvuPoB8

TECHNOLOGY

Revolutionizing Vehicle Safety

The Significance, Functionality and Future of Anti-Lock Braking System (ABS)

By Brian Yam

1.0Introduction

Anti-LockBrakingSystem(ABS)standsasapillarofmodernvehiclesafety.Oftenunseenandunderappreciated,ABSplays avitalroleinensuringthateveryjourneyissaferandmoresecure.Thisarticleevaluatesitssignificanceinrevolutionising transportsafety,consideringitslimitationsandfutureadvancements.

2.0EffectivenessinReducingCrashRisks

InastudyconductedbyGeneralMotors,theinfluenceofanti-lockbrakingsystemsonrelativecrashriskunderadverse andnormalconditionswasinvestigated[1].Thestudyusedseven1992GeneralMotorspassengervehicleswhichhave ABSasstandardequipmentandanalysedcrashesbetween1992-1993inTexasandMissouri.AssumingthatABSis associatedwithnodifferenceincrashriskondryroadsandthatdriversdidnotusetheimprovedbrakingprovidedbyABS fortravellingathigherspeeds,itisconcludedthatABSreducesoverallcrashriskby(3±1)%,reducescrashriskonwet roadsby(13±4)%,reducescrashriskwhenitisrainingby(13±5)%andreducespedestriancrashesby(34±15)%.This indicateshowABSmakesdrivingmuchsafer,especiallyintherainwhentheslipperyroadsmakeiteasytolockup.

3.0LockingUp

InordertounderstandwhatABSevenisandhowitworks,wemustfirstdiveinto themechanismsofbraking Slowingdownyourvehiclereliesonthefriction betweenthebrakepadsandthewheels Whenyouapplythebrakesfirmly,the brakepadsexertsignificantpressureonthespinningwheel,aimingto decelerateit However,thereareinstanceswhenthispressurebecomes excessive,causingthewheeltolockup[3] Inotherwords,whenthebrakepads aretightlypressedagainstthedrumordisc,thewheelcomestoasuddenhalt Whenthewheellocksup,itlosesitsabilitytorotatefreely,leadingtoalossof tractionwiththeroadsurface.Thissituationcanbeparticularlyhazardous becauseithampersyourabilitytosteerthevehicle.Withouttheabilityto maintaincontroloverthedirectionofthevehicle,itbecomessusceptibleto skiddingorveeringoffitsintendedpath.Inanutshell,whenadriverbrakestoo hardwithoutABS,thisresultsinthevehicleflyinguncontrollablyinacertain direction,muchliketryingtostopyourselffrommovingwhenyouareiceskating inapairofNikes.Asweallknow,iceskatinginapairofNikesresultsinan inevitablebrokenhand.Inthecaseofautomobiles,brakingwithoutABSalmost alwaysleadstotrafficaccidents.

4.0HowDoesABSWork?

Topreventthispotentiallyhazardoussituation,theAnti-lockBrakingSystem(ABS)employsitsimpressivetechnology.For acomprehensiveunderstandingoftheintricateworkingsofABS,itiscrucialtodelveintothefunctionsofABSandits individualcomponents.

4.1SpeedSensors

TheABSwheelspeedsensorsplayacrucialroleinmonitoringthespeedofeachwheelanddeterminingthenecessary decelerationoraccelerationforthatspecificwheel.Thesesensorsconsistofessentialcomponents,includinga permanentmagnet,coil,andaringwithV-shapedteethcalledatonewheel.Asthetonewheelrotates,eachtoothpasses infrontofthepermanentmagnet,causingachangeinthemagneticfluxitgenerates.Consequently,thischangeinduces voltagesinthecoilatafrequencydirectlyproportionaltothespeedofthewheel.Thecontrollerreceivesthesesignals fromthegeneratedvoltages,allowingittoassessthewheel'saccelerationanddecelerationaccurately[3].

4.2MasterCylindersandValves

Themastercylinderservesasadeviceresponsibleforpumping brakefluidandcomprisesthreeessentialcomponents:apiston, brakefluid,andareturnspring[2].Connectedtothebrakepedal viathepistonrod,themastercylinderfunctionswhenthedriver appliespressuretothebrakepedal.Asaresult,thepistonwithin themastercylindercompressesthebrakefluid(atypeof hydraulicfluidusedinhydraulicbrakingsystemstotransferforce intopressure),enablingittotransmittheappliedforce. Additionally,themastercylinderisconnectedtoanoilreservoir, whichregulatesandmaintainstheappropriatelevelofbrakefluid withinthesystem

WithintheABSsystem,eachbrakelineisequippedwithavalve thattheABScontrols Dependingonthespecificsystem,this valvecanbesettothreedistinctpositions

Inthefirstposition,thevalveremainsopen,allowingthepressure generatedbythemastercylindertopassthroughtothebrake, enablingeffectivebraking

Inthesecondposition,thevalveobstructstheline,creatinga separationbetweenthebrakeandthemastercylinder. Consequently,thebrakepressuredoesnotincreasebeyonda certainpoint.Thispositionisactivatedwhenthedriverapplies thebrakeswithmoreforcefulpressure.

Inthethirdposition,thevalvereleasesaportionofthepressurefromthebrake Thisprocessisrepeateduntilthevehicle comestoacompletestop Thebrakevalvesregulateandcontrolthepressuredeliveredfromthemastercylindertothe brakes,ensuringasmoothandcontrolledbrakingexperience

4.3ElectronicControlUnit

TheprimaryfunctionoftheElectronicControlUnit(ECU)istoreceive,amplify,andfiltersignalsfromvarioussensorsto calculatecrucialvehicleparameterssuchasspeed,rotation,andacceleration Additionally,theECUutilisesthespeedsof twodiagonallyopposingwheelstoestimatethevehicle'soverallspeed Bycomparingthisreferencespeedwiththe speedofeachindividualwheel,theECUisabletodeterminetheslip(differencebetweentheactualspeedofavehicle's wheelandthedesiredspeedduringbrakingoracceleration Thisdifferenceoccurswhenawheelspinsfasterorslower duetolowtraction)ofeachwheel Intheeventofwheelslideoracceleration,thesignalserveralertstheECU Consequently,thecontrollertakesactionbylimitingthebrakeforcethroughElectronicBrakeforceDistribution(EBD)and activatingtheABSmodulator

Onceactivated,theABSmodulatorcomesintoplaybycontrollingthebrakingvalves,alternatelyturningthemonandoff toadjustthebrakepressure,modulatingthebrakepressureinthebrakecylindersofeachindividualwheel.

4.4Howdoesthisallcometogether?

TheECUreadsthesignalfromeachwheel'sspeedsensor. Whenthedriverappliesthebrakessuddenly,thewheel deceleratesrapidly,whichcanleadtowheellock-up.TheECU receivesasignalindicatingthissuddendecreaseinwheel speedandtransmitsittoavalve.Thisactioncausesthevalveto close,reducingthepressureonthebrakepadandpreventing wheellock-up.

Asthewheelacceleratesagain,asignalissenttothecontroller. Inresponse,thecontrolleropensthevalve,increasingthe pressureonthebrakepadandengagingthebrakes.This processrepeats,reducingthewheel'sspeedandattemptingto bringthevehicletoastop.

Insituationswherethedriverappliesthebrakesmoreforcefully,theprocessofapplyingandreleasingthebrakesoccurs upto15timespersecond.Thisrapidmodulationpreventswheellock-upandeliminatesthevehicle'stendencytoskid. WithABSinoperation,thedrivercansteerthecarwhilebraking,significantlyreducingtheriskofaccidents.

5.0TheHistoryofABS

ThefirstapplicationofABSwasinthe1950s,whendiscbrakepioneerDunlopcameupwithasystemthatcouldimprove theRoyalAirForce’sbrakingperformancebyupto30%.Thesameantilockbrakesystemwasalsoputonmotorbike prototypesandbythe60s,FergusonResearchuseditontheworld'sfirstfour-wheeldriveFormulaOnecar,theClimaxpoweredP99.Afterthat,thetaskofmakingABScheapandreliableenoughformainstreamautomotiveproductionfellto theGermans.In1978,Mercedes-Benzofferedthefirstproductioncarwithelectronicfour-wheelmulti-channelABS, launchingasafetyandperformancerevolution.Comingbacktothepresentday,ithasbeenclosetohalfadecadesince ABSwasfirstintroduced--asanincreasinglyadvancedtechnology,therearegreatanticipationsforwhatitsnextevolution willbring.

6.0FutureDevelopmentofABS

6 1 Current Limitations

Valve clogging is the most serious issue with ABS. The valve becomes difficult to open, close, or change position as it becomes clogged. When the valve is inoperable, the system is unable to modulate the valves and control the pressure to the brakes. While engineers are trying to improve this problem, the only resort to this now is to take out the ABS controller and all electronics and replace it However, it is quite expensive [4] It should also be mentioned that ABS do not work effectively in areas with bad road conditions.

6.2TheFutureofABS

Brakesystemstodatehaveprimarilybeenmechanicalsystemswithvacuumbrakeboostersandhydraulicpower transmissionfromthebrakepedaltothewheelbrake(entailingpressuregeneration,valves,lines,brakecallipersanddrum brakes).ElectronicsafetysystemssuchasABSensurethatbrakesproactivelycontributetodrivingsafetyinborderline situationsevenwithoutdriverintervention.Atthesametime,brakesmustnowalsocontributetovehicleefficiency–in otherwords,helppreventCO2emissions–and,infuture,reduceparticulateemissionsduringfrictionbraking.Fornow,a featurecalledRegenerativeBrakingisbeingintroducedtobepartofelectriccars’anti-lockbrakingsystem.Theproposed electronicbrakingsystemforelectricvehiclesintegratestheregenerativebrakingandautomaticallycontrolled mechanicalbrakingtogether.Thisbrakingsystemcanrecovermostofthebrakingenergy.Therefore,theenergy efficiencyofthevehiclecanbesignificantlyimproved.

Thelatestadvanceknownas“ElectronicBrakePowerDistribution”isproductiveirrespectiveofwhetherstreetconditions arefrosty,watery,orhoweverunfavourabletheconditionsare.Italsoimprovesvehiclestabilitybyincorporatingutilityina controlunit.

7.0Conclusion

Inconclusion,theAnti-lockBrakingSystem(ABS)standsasapillarofmodernvehiclesafety,effectivelyreducingcrash risksandprovidingdriverswithenhancedcontrolandmanoeuvrability.Throughitsintricatecomponentsand technology,ABSpreventswheellock-up,improvesbrakingperformanceonwetroads,andreducesoverallcrashrisk. Despiteitshistoricalrootsandadvancements,futuredevelopmentsinABSaimtoaddressissuessuchasvalveclogging andintegrateregenerativebrakingforimprovedenergyefficiency.WhileABSmayhavelimitationsincertainroad conditions,ongoingadvancementslikeElectronicBrakePowerDistributionstrivetoovercomethesechallengesand ensuresaferandmorestabledrivingexperiences.ABShasrevolutionisedbrakingsystems,makingdrivingsaferand settingthestageforfurtheradvancementsinvehiclesafety.

8.0Bibliography

[1]Evans,Leonard “ABSandRelativeCrashRiskUnderDifferentRoadway,Weather,andOtherConditions”SAE Transactions,vol 104,1995,pp 676–86 JSTOR,http://wwwjstororg/stable/44612235 Accessed11Mar 2024

[2]Automotive,ChristianBrothers Anti-LockBrakingSystem |InternationalJournalofInnovativeResearchin Engineering&Management.https://acspublisher.com/journals/index.php/ijirem/article/view/11279.Accessed11Mar. 2024.

[3]Musa,Abu.“HowDoesABSWork?ACompleteGuide.”SuzukiFortMotors(blog),December14, 2021.https://suzukifortmotors.com/how-does-abs-work/.

[4]PopularMechanics.“YourFaultyAnti-LockBrakesAreNotanImpossibleFix,”July7, 2021.https://www.popularmechanics.com/cars/car-technology/a461/how-to-fix-anti-lock-brakes/.