中国历代园林图文精选 生物科学生物技术科技英语阅读精选(1)_图文

中国历代园林图文精选生物科学生物技术科技英语阅读精选(1)_图文导读：就爱阅读网友为您分享以下“生物科学生物技术科技英语阅读精选(1)_图文”的资讯，希望对您有所帮助，感谢您对92to.com的支持!inhibitors.Forexample,theG9ainhibitorUNC0638reactivatessilentretroviralinserts3.Thismaybeusefulinthecontextofcellularreprogrammingstrategies,butitraisessafetyissuesabouttheuseofhistonemethyltransferaseinhibitorsinpatients.Muchremainstobelearnedabouthistonemethyltransferasesandtheirpotentialastherapeuticsand9 diagnostics.Welookforwardwithgreatinteresttofurtherdevelopments,especiallythefirstclinicalstudiesofhistonemethyltransferaseinhibitors,whichmaybeginsoonHowCellsCopewithObesityFreelanceScienceWriter,SanDiego,California,UnitedStatesofAmericaCitation:SedwickC(2011)HowCellsCopewithObesity.PLoSBiol9(6):e1001077.doi:10.1371/journal.pbio.1001077Published:June7,2011Copyright:?2011CaitlinSedwick.Thisisanopen-accessarticledistributedunderthetermsoftheCreativeCommonsAttributionLicense,whichpermitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited.Currently,morethan2.7millionAmericanadultsarediagnosedasobeseeachyear.Manyofthesepeople9 sufferfromadisorderknownasmetabolicsyndrome,whichincludessymptomslikehypertensionandelevatedbloodcholesterol.Theyarealsoatriskfordevelopingadditionaldiseasessuchasheartdiseaseanddiabetesmellitus.Infact,obesitymaybeamajorcauseofalltheseproblems?thequestionis,why?That'sthequestionKirsiH.Pietil?inen,AntonioVidal-Puig,MatejOre?i?,andcolleaguessetouttoaddressintheirpaperpublishedinthismonth'sPLoSBiology.Oneprominenttheoryexplaininghowobesitycoulddriveadvanceddiseasestatesisthe“adiposetissueexpandability”hypothesis.Thistheoryisbasedontheideathatasexcessfatisaddedtothebody,itsfatcompartment(adiposetissue)expandsasmorefat-storingcellsaremadeandexistingonesincreaseinsize.However,expandabilityofthefatcompartmentisfinite;likeawaterballoon,thefatcompartmentcanonlyexpandsomuchbeforeleaksdevelop.Forthebody,“leaks”inthefatcompartmentmanifestasdepositionsoffatintissueswhere9 itspresencecanbedisruptivetonormalfunction—ashappensinmorbidlyobeseindividuals.But,lowerlevelsofexpansionaretolerated—possiblyduetocompensatorymechanisms—sothattissuesandsystemscanfunctionnormally.Sowhatisgoingoninthebodywhenthefatcompartmentsareexpandedbutnotyetfull?Toexplorethisquestioninhumans,theauthorsdecidedtocompareadiposetissueandhealthparametersamongstseveralsetsofmonozygotictwins.Ineachtwinpair,onetwinwasobese(butstillhealthy,i.e.,notmorbidlyobese),whiletheothertwinexhibitedanormalbodymassindex.BecausemonozygotictwinssharethesameDNAandearlyupbringing,theimpactofthesefactorsonadultbodymassphenotypesiscontrolledfor,leavingotherfactorssuchasadultdietandlifestylechoicesasthemajorremainingvariables.Whentheauthorscompareddietaryintakewithintwinsets,theyfoundthatobesetwinshadloweramountsofpolyunsaturatedfattyacidsintheirdietsthandidtheir9 non-obesecounterparts.Thekindsoffatsapersoneatscanaffectwhattypesoflipidsarepresentinthebody,sotheauthorsnextcomparedthelipidcontentofobeseversusnon-obesetwins'adiposetissue.Infact,theyfoundtheobesepeoplehadhigheramountsofcertaintypesofphospholipidsintheiradiposetissuesthandidtheirnon-obeseco-twins.Thisfindingisinterestingbecausecellmembranesareprimarilycomposedoflipids,anddifferentlipidscanaltermembranes'physicalproperties.Forexample,lipidswithlargerheadgroups,orlongerorbranchedsidechainsarefoundtopacklesstightlyinmembranes,makingthemembranesthathostthemmorefluid.Whentheauthorsusedcomputerstomodeltheeffectthesedifferentlipidshaveonadiposecellmembranes,theyfoundthatthenewlipidsobservedinobesetwins'adiposecellsbalanceeachotherinsuchawaythatmembranefluidityoverallisunaffected.Theauthorsconcludedthatlipidcontentchangesinobese9 individualsmightactuallybeanadaptationthatservestopreservemembranefunctionasthecellsexpand.However,additionalanalysessuggestedthatthisadaptationcanonlygosofar,andbreaksdowninthemorbidlyobese.生物科学生物技术科技英语阅读精选（1）精选自Nature﹑PloSBiology等顶尖杂志。图文表并茂。生物科学﹑生物技术﹑生物工程的参考资料。可用于考研参考，课外阅读练习，论文写作参考，专业英语学习的资料。TherapeutictargetsincancercellmetabolismandautophagyNatureBiotechnology30,671–678(2012)doi:10.1038/nbt.22859 Publishedonline10July2012AbstractThemetabolismofcancercellsisreprogrammedbothbyoncogenesignalingandbydysregulationofmetabolicenzymes.Theresultingalteredmetabolismsupportscellularproliferationandsurvivalbutleavescancercellsdependentonacontinuoussupplyofnutrients.Thus,manymetabolicenzymeshavebecometargetsfornewcancertherapies.Recently,twoprocesses—expressionofspecificisoformsofmetabolicenzymesandautophagy—havebeenshowntobecrucialfortheadaptationoftumorcellstochangesinnutrientavailability.Anincreasingnumberofapprovedandexperimentaltherapeuticstargetthesetwoprocesses.Abetterunderstandingofthemolecularbasisofcancer-associatedmetabolicchangesmayleadtoimprovedcancertherapies.9 Activemetabolicpathwaysinproliferatingcellsinvolvingglucoseandglutaminecatabolismareinterconnectedandlinkedtomacromolecularsynthesisandenergybalance.Keymetabolicenzymesdiscussedinthetext(showninblue)areactivelyinvestigatedastherapeutictargetsforcancertreatment.Metabolicenzymestargetedbyregisteredagentsareshowninred.ACL,ATPcitratelyase;αKG,α-ketoglutarate;DH,dehydrofolate;DHFR,dehydrofolatereductase;dTMP,deoxythymidinemonophosphate;dUMP,deoxyuridinemonophosphate;F-2,6-BP,fructose-2,6-bisphosphate;F6P,fructose-6-phosphate;FBP,fructose-1,6-bisphosphate;FH,fumaratehydratase;G6P,glucose-6-phosphate;GLS,glutaminase;HK2,hexokinase2;IDH,isocitratedehydrogenase;LDHA,lactatedehydrogenaseA;MCT1,4,monocarboxylatetransporter1,4;ME,malicenzyme;OAA,oxaloacetate;PDH,pyruvatedehydrogenasecomplex;PDK,pyruvatedehydrogenasekinase;9 PEP,phosphoenolpyruvate;PFK,phosphofructokinase;PGAM,phosphoglyceratemutase;PHGDH,phosphoglyceratedehydrogenase;PKM2,pyruvatekinaseM2isoform;R5P,ribose-5-phosphate;SDH,succinatedehydrogenase;TCA,tricarboxylicacid;THF,tetrahydrofolate;TYMS,9