简介：AbstractBackground:Subarachnoid hemorrhage (SAH), an acute cerebrovascular accident, features with its high death and disability rate. Sirtuin3 (SIRT3) is a NAD+ dependent deacetylase which mainly located in mitochondria. Reduced SIRT3 function was indicated to involve in many disorders of central nervous system. Herein, we aimed to explore the neuroprotective effects of SIRT3 on SAH and to furtherly explore the underlying mechanisms.Methods:Adult C57BL/6 J male mice (8-10 weeks) were used to establish SAH models. The pharmacological agonist of SIRT3, Honokiol (HKL), was injected in an intraperitoneal manner (10 mg/kg) immediately after the operation. Brain edema and neurobehavioral score were assessed. Nissl staining and FJC staining were used to evaluate the extent of neuronal damage. The changes of mitochondria morphology were observed with transmission electron microscopy. Western blot was used for analyzing the protein level of SIRT3 and the downstream signaling molecules.Result:SIRT3 was downregulated after SAH, and additional treatment of SIRT3 agonist HKL alleviated brain edema and neurobehavioral deficits after SAH. Additionally, electron microscopy showed that HKL significantly alleviated the morphological damage of mitochondria induced by SAH. Further studies showed that HKL could increase the level of mitochondrial fusion protein Mfn1 and Mfn2, thus maintaining (mitochondrial morphology), protecting mitochondrial function and promoting neural survival. While, additional Compound C (CC) treatment, a selective AMPK inhibitor, abolished these protective effects.Conclusions:Activation of SIRT3 protects against SAH injury through improving mitochondrial fusion in an AMPK dependent manner.

简介：在源于mitochondrial机能障碍的氧化phosphorylation的改变长被假设了涉及tumorigenesis。线粒体最近被显示了在调整规划房间死亡和房间增长起一个重要作用。而且，mitochondrialDNA(mtDNA)变化在各种各样的癌症房间被发现了。然而，在tumorigenesis的这些mtDNA变化的角色仍然保持大部分未知。这评论集中于基本mitochondrial遗传，mtDNA变化和与癌症联系的结果的mitochondrial机能障碍。潜在的分子的机制，调停从mtDNA变化的致病和到tumorigenesis的mitochondrial机能障碍也被讨论。

简介：“FusionWorld”科技展示体验中心是英国设计公司METStudio为新加坡科技研究局（A＊Star）的科学工程委员会（SERC）所设计的,位于启汇城的办公地点，用于展示该委员会的精选技术作品，以吸引潜在的客户和启汇城内的学生购买群体。

简介：Basedonthefirstlawofthermodynamicsandthethermaldiffusionequation,thededucedtheoreticalmodelofmitochondrialthermogenesissatisfiestheLaplaceequationandisaspecialcaseofthethermaldiffusionequation.Themodelsettlesthelong-standingquestionoftheabilitytoincreasecellulartemperaturebyendogenousthermogenesisandexplainsthethermogeniccharacteristicsofbrownadipocytes.Themodelandcalculationsalsosuggestthatthenumberoffreeavailableprotonsisthemajorlimitingfactorforendogenousthermogenesisanditsspeed.

简介：人的耳朵是为正常通讯的听觉的一台精细的感觉仪器，并且它的合适的工作高度依赖于mitochondrialoxidativephosphorylation。为nonsyndromic和aminoglycoside-inducedhearing损失的第一mitochondrial点突变在1993被识别。从那以后，很多个继承mitochondrial变化在听见损失被含有。大多数为联系mitochondrialdisorder的听觉损失负责的分子的缺点是在12SrRNA基因和tRNA基因的变化。在这评论，在对正常听觉机制和mitochondrial的短描述以后，我们构画出在联系聋的mitochondrialmutations的鉴定被做了的最近的进展，并且讨论mitochondrial机能障碍怎么贡献听觉损失。

简介：MitochondrialtRNAmutationsareoneoftheimportantcausesofbothsyndromicandnon-syndromicdeafness.Ofthose,syndromicdeafness-associatedtRNAmutationssuchastRNALeu(UUR)3243A>Gareoftenpresentinheteroplasmy,whilenon-syndromicdeafness-associatedtRNAmutationsincludingtRNASer(UCN)7445A>Gareofteninhomplasmyorinhighlevelsofheteroplasmy.ThesetRNAmutationsaretheprimarymutationsleadingtohearingloss.However,othertRNAmutationssuchastRNAThr15927G>AandtRNASer(UCN)7444G>AmayactinsynergywiththeprimarymitochondrialDNAmutations,modulatingthephenotypicmanifestationoftheprimarymitochondrialDNAmutations.ThesestRNAmutationscausestructuralandfunctionalalteration.AfailureintRNAmetabolismcausedbythesetRNAmutationsimpairedmitochondrialtranslationandrespiration,therebycausingmitochondrialdysfunctionsresponsiblefordeafness.Thesedataoffervaluableinformationfortheearlydiagnosis,managementandtreatmentofmaternallyinheriteddeafness.

简介：Performancesrequired:prospecttobeadoptedinDEMO.ShieldingforV.V.andTFCinITER.Designprinciples:thepeaktemperatureandstressshouldnotexceedtechnicallimits.Thestructureoftestblanketmodules(TBM)shouldbesimpleforeasyfabrication,andTBMshouldberobustforreliability.

简介：Themitochondrial12SrRNAhasbeenshowntobethehotspotformutationsassociatedwithbothaminoglycoside-inducedandnon-syndromichearingloss.Ofallthemutations,thehomoplasmicA1555GandC1494Tmutationsatahighlyconserveddecodingregioninthe12SrRNAhavebeenassociatedwithaminoglycoside-inducedandnon-syndromichearinglossinmanyfamiliesworldwide.TheA1555GorC1494Tmutationisexpectedtoformnovel1494C-G1555or1494U-A1555base-pairatthehighlyconservedA-siteof12SrRNA.ThesetransitionsmakethesecondarystructureofthisRNAmorecloselyresemblethecorrespondingregionofbacterial16SrRNA.Thus,thenewU-AorG-Cpairin12SrRNAcreatedbytheC1494TorA1555Gtransitionfacilitatesthebindingofaminoglycosides,therebyaccountingforthefactthattheexposuretoaminoglycosidescaninduceorworsenhearinglossinindividualscarryingthesemutations.Furthermore,thegrowthdefectandimpairmentofmitochondrialtranslationwereobservedincelllinescarryingtheA1555GorC1494Tmutationinthepresenceofhighconcentrationofaminoglycosides.Inaddition,nuclearmodifiergenesandmitochondrialhaplotypesmodulatethephenotypicmanifestationoftheA1555GandC1494Tmutations.TheseobservationsprovidethedirectgeneticandbiochemicalevidencesthattheA1555GorC1494TmutationisapathogenicmtDNAmutationassociatedwithaminoglycoside-inducedandnonsyndromichearingloss.Therefore,thesedatahavebeenprovidingvaluableinformationandtechnologytopredictwhichindividualsareatriskforototoxicity,toimprovethesafetyofaminoglycosideantibiotictherapy,andeventuallytodecreasetheincidenceofdeafness.

简介：Stressinducedtheseriousdisorderofcardiacfunctionandcardiovasculardiseases.Apoptosisisthecellularbasisinstressinducedcardiacinjury.Inourpreviousstudywefoundthatmanystressorsresultedinmitochondrialdamage.Itiscertainthatmitochondriaisimportantmediatorintriggeringapoptoticcelldeath,butthemechanism,bywhichthestressinducedmitochondrialinjuryleadstocardiomyocyteapoptosis,remainsunclear.Wedesignedthepresentstudytoinvestigatethechangesofthemitochondriaincardiomyocytesundergoingstressanditsroleininducingapoptosis.Herewereportedthatstresschangedthemembranefluidityofmitochondriaandinducedthelipidperoxidationofmitochondrialmembranein

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简介：Thefastions,producedinD-3Hefusionplasma,arethe14.7MeVprotonsand3.6MeVαparticles.Becausetheirslowingdowntimesarefinite,therefore,theydevelopacertainamountofadditionalbeta(fir)whichhastobesupportedbythemagneticfield.

简介：Asthebasicconditionsforlaserinertialconfinementfusion（ICF）research,thetargetsarerequiredtobewellspecifiedandelaboratelyfabricated.Becauseofthecharacteristicsofthetargets,theresearchandfabricationprocessisasystematicallytoughtask,whichneedsfundamentalanddeepinsightsintofilmdeposition,mechanicalmachining,precisemeasurementandassembly,etc.Asaresult,knowledgeofmaterialscience,physics,mechanicalaswellaselectronicsisanecessityfortargetresearchers.Inthispaper,wegiveintroductionstothestateofartontargetfabricationforICFresearchatResearchCenterofLaserFusion（RCLF）inChina.

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简介：Thereisaccumulatingevidencethatcysteinesulfenation（cys-SOH）inproteinsplaysanimportantroleincellularresponsetooxidativestress.Thepurposeofthepresentstudywastoidentifymitochondrialproteinsthatundergochangesincys-SOHduringaging.Studieswereconductedinratswhentheywere5or30monthsofage.FollowingblockingoffreeproteinthiolswithN-ethylmaleimide,proteinsulfenicacidswerereducedbyarsenitetofreethiolgroupsthatweresubsequentlylabeledwithbiotin-maleimide.Sampleswerethencomparativelyanalyzedbytwo-dimensionalWesternblots,andproteinsshowingchangesinsulfenationwereselectivelyidentifiedbymassspectrometrypeptidesequencing.Asaresult,fiveproteinswereidentified.Proteinsshowinganage-relateddecreaseinsulfenationincludepyruvatecarboxylaseandpyruvatedehydrogenase;whilethoseshowinganage-relatedincreaseinsulfenationincludeaconitase,mitofilin,andtubulin（α-1）.Resultsofthepresentstudyprovideageneralpictureofmitochondrialproteinsulfenationinbrainoxidativestressandimplicatetheinvolvementofproteinsulfenationinoveralldeclineofmitochondrialfunctionduringbrainaging.

简介：MutationsinmitochondrialtRNAgeneshavebeenshowntobeassociatedwithmaternallyinheritedsyn-dromicandnon-syndromicdeafness.Amongthose,mutationssuchastRNALeu(UUR)3243A>Gassociatedwithsyndromicdeafnessareoftenpresentinheteroplasmy,andthenon-syndromicdeafness-associatedtRNAmu-tationsincludingtRNASer(UCN)7445A>Gareofteninhomoplasmyorinhighlevelsofheteroplasmy.ThesetRNAmutationsaretheprimaryfactorsunderlyingthedevelopmentofhearingloss.However,othertRNAmutationssuchastRNAThr15927G>AandtRNASer(UCN)7444G>Aareinsufficienttoproduceadeafnessphe-notype,butalwaysactinsynergywiththeprimarymitochondrialDNAmutations,andcanmodulatetheirphenotypicmanifestation.ThesetRNAmutationsmayalterthestructureandfunctionofthecorrespondingmitochondrialtRNAsandcausefailuresintRNAsmetabolism.Thereby,theimpairmentofmitochondrialproteinsynthesisandsubsequentdefectsinrespirationcausedbythesetRNAmutations,resultsinmitochon-drialdysfunctionsandeventuallyleadstothedevelopmentofhearingloss.Here,wesummarizedthedeaf-ness-associatedmitochondrialtRNAmutationsanddiscussedthepathophysiologyofthesemitochondrialtRNAmutations,andwehopethesedatawillprovideafoundationfortheearlydiagnosis,management,andtreatmentofmaternallyinheriteddeafness.

简介：ToinvestigategeneticmechanismsofhighaltitudeadaptationsofnativemammalsontheTibetanPlateau,wecomparedmitochondrialsequencesoftheendangeredPantholopshodgsoniiwithitslowlanddistantrelativesOvisariesandCaprahircus,aswellasothermammals.ThecompletemitochondrialgenomeofP.hodgsonii(16,498bp)revealedasimilargeneorderasofothermammals.Becauseoftandemduplications,thecontrolregionofP.hodgsoniimitochondrialgenomeisshorterthanthoseofO.ariesandC.hircus,butlongerthanthoseofBosspecies.PhylogeneticanalysisbasedonalignmentsoftheentirecytochromebgenessuggestedthatP.hodgsoniiismorecloselyrelatedtoO.ariesandC.hircus,ratherthantospeciesoftheAntilopinaesubfamily.TheestimateddivergencetimebetweenP.hodgsoniiandO.ariesisabout2.25millionyearsago.FurtheranalysisonnaturalselectionindicatedthattheCOXI(cytochromecoxidasesubunitI)genewasunderpositiveselectioninP.hodgsoniiandBosgrunniens.Consideringthesameclimatesandenvironmentssharedbythesetwomammalianspecies,weproposedthatthemitochondrialCOXIgeneisprobablyrelevantforthesenativemammalstoadaptthehighaltitudeenvironmentuniquetotheTibetanPlateau.

简介：Aminoglycosides(AmAn)arewidelyusedfortheirgreatefficiencyagainstgram-negativebacterialinfections.However,theycanalsoinduceototoxichearingloss,whichhasaffectedmillionsofpeoplearoundtheworld.Aspreviouslyreported,individualsbearingmitochondrialDNAmutationsinthe12SrRNAgene,suchasm.1555A>Gandm.1494C>T,aremorepronetoAmAn-inducedototoxicity.Thesemutationscausehumanmitochondrialribosomestomorecloselyresemblebacterialribosomesandenableastrongeraminoglycosideinteraction.Consequently,exposuretoAmAncaninduceorworsenhearinglossintheseindividuals.Furthermore,awiderangeofseverityandpenetranceofhearinglosswasobservedamongfamiliescarryingthesemutations.StudieshaverevealedthatthesemitochondriamutationsaretheprimarymolecularmechanismofgeneticsusceptibilitytoAmAnototoxicity,thoughnuclearmodifiergenesandmitochondrialhaplotypesareknowntomodulatethephenotypicmanifestation.

简介：MtDNAwassuccessfullyextractedfromtenindividualbones(femurs)inthetombsofancientJushiinTurfanbasin,datedbacktotheyearabout3000-2500yearsago.Bymeansoffouroverlappingprimers,wegotnucleotidesequenceofthe218bplength.AncientmtDNAwasanalyzedbythesequencingofhypervariableregionⅠofthemtDNAcontrolregion.Theresultshowsthat9haplotypeswith24polymorphicsiteswereobtained.ThephylogeneticanalysisindicatedthatMongoliansandAltaiarethepopulationgeneticallyclosesttotheJushigroupsandJushimtDNApoolbeinganadmixtureofeasternAsianandEuropeanlineages.SoourpreliminarydataimplythatanancientminglingofEuro-AsianpopulationhadexistedinTurfanbasinpriortotheearlyIronAge.