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RWALLISMORETHAN2CMINTHICKNESSNORMALIS1TO15CMINTHESPECIMENSHOWINGNECROSIS,THETRANSMURALLIGHTAREAINTHEPOSTEROLATERALLEFTVENTRICLEREPRESENTSANACUTEMYOCARDIALINFARCTIONALLTHREETRANSVERSESECTIONSHAVEBEENSTAINEDWITHTRIPHENYLTETRAZOLIUMCHLORIDE,ANENZYMESUBSTRATETHATCOLORSVIABLEMYOCARDIUMMAGENTAFAILURETOSTAINISDUETOENZYMELEAKAGEAFTERCELLDEATHHYPERPLASIAHYPERPLASIAISANINCREASEINTHENUMBEROFCELLSINANORGANORTISSUE,USUALLYRESULTINGININCREASEDVOLUMEOFTHEORGANORTISSUEALTHOUGHHYPERPLASIAANDHYPERTROPHYARETWODISTINCTPROCESSES,FREQUENTLYBOTHOCCURTOGETHER,ANDTHEYMAYBETRIGGEREDBYTHESAMEEXTERNALSTIMULUSFORINSTANCE,HORMONEINDUCEDGROWTHINTHEUTERUSINVOLVESBOTHINCREASEDNUMBERSOFSMOOTHMUSCLEANDEPITHELIALCELLSANDTHEENLARGEMENTOFTHESECELLSHYPERPLASIATAKESPLACEIFTHECELLULARPOPULATIONISCAPABLEOFSYNTHESIZINGDNA,THUSPERMITTINGMITOTICDIVISIONBYCONTRAST,HYPERTROPHYINVOLVESCELLENLARGEMENTWITHOUTCELLDIVISIONHYPERPLASIACANBEPHYSIOLOGICORPATHOLOGICPHYSIOLOGICHYPERPLASIAPHYSIOLOGICHYPERPLASIACANBEDIVIDEDINTO1HORMONALHYPERPLASIA,WHICHINCREASESTHEFUNCTIONALCAPACITYOFATISSUEWHENNEEDED,AND2COMPENSATORYHYPERPLASIA,WHICHINCREASESTISSUEMASSAFTERDAMAGEORPARTIALRESECTIONHORMONALHYPERPLASIAISBESTEXEMPLIFIEDBYTHEPROLIFERATIONOFTHEGLANDULAREPITHELIUMOFTHEFEMALEBREASTATPUBERTYANDDURINGPREGNANCYANDTHEPHYSIOLOGICHYPERPLASIATHATOCCURSINTHEPREGNANTUTERUSTHECLASSICALILLUSTRATIONOFCOMPENSATORYHYPERPLASIACOMESFROMTHEMYTHOFPROMETHEUS,WHICHSHOWSTHATTHEANCIENTGREEKSRECOGNIZEDTHECAPACITYOFTHELIVERTOREGENERATEASPUNISHMENTFORHAVINGSTOLENTHESECRETOFFIREFROMTHEGODS,PROMETHEUSWASCHAINEDTOAMOUNTAIN,ANDHISLIVERWASDEVOUREDDAILYBYAVULTURE,ONLYTOREGENERATEANEWEVERYNIGHT1THEEXPERIMENTALMODELOFPARTIALHEPATECTOMYHASBEENESPECIALLYUSEFULINEXAMININGTHEMECHANISMSTHATSTIMULATEPROLIFERATIONOFRESIDUALLIVERCELLSANDREGENERATIONOFTHELIVERSIMILARMECHANISMSARELIKELYINVOLVEDINOTHERSITUATIONSWHENREMAININGTISSUEGROWSTOMAKEUPFORPARTIALTISSUELOSSEG,AFTERUNILATERALNEPHRECTOMY,WHENTHEREMAININGKIDNEYUNDERGOESCOMPENSATORYHYPERPLASIAPAGE6PAGE7MECHANISMSOFHYPERPLASIAHYPERPLASIAISGENERALLYCAUSEDBYINCREASEDLOCALPRODUCTIONOFGROWTHFACTORS,INCREASEDLEVELSOFGROWTHFACTORRECEPTORSONTHERESPONDINGCELLS,ORACTIVATIONOFPARTICULARINTRACELLULARSIGNALINGPATHWAYSALLTHESECHANGESLEADTOPRODUCTIONOFTRANSCRIPTIONFACTORSTHATTURNONMANYCELLULARGENES,INCLUDINGGENESENCODINGGROWTHFACTORS,RECEPTORSFORGROWTHFACTORS,ANDCELLCYCLEREGULATORS,ANDTHENETRESULTISCELLULARPROLIFERATIONINHORMONALHYPERPLASIA,THEHORMONESMAYTHEMSELVESACTASGROWTHFACTORSANDTRIGGERTHETRANSCRIPTIONOFVARIOUSCELLULARGENESTHESOURCEOFGROWTHFACTORSINCOMPENSATORYHYPERPLASIAANDTHESTIMULIFORTHEPRODUCTIONOFTHESEGROWTHFACTORSARELESSWELLDEFINEDTHEINCREASEINTISSUEMASSAFTERSOMETYPESOFCELLLOSSISACHIEVEDNOTONLYBYPROLIFERATIONOFTHEREMAININGCELLSBUTALSOBYTHEDEVELOPMENTOFNEWCELLSFROMSTEMCELLSFORINSTANCE,INTHELIVER,INTRAHEPATICSTEMCELLSDONOTPLAYAMAJORROLEINTHEHYPERPLASIATHATOCCURSAFTERHEPATECTOMYBUTTHEYMAYPARTICIPATEINREGENERATIONAFTERCERTAINFORMSOFLIVERINJURY,SUCHASCHRONICHEPATITIS,INWHICHTHEPROLIFERATIVECAPACITYOFHEPATOCYT
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