简介：Theperitonealstromaltissuewhichprovidesarichsourceofgrowthfactorsandchemokinesisafavorableenvironmentfortumorproliferation.Thepathophysiologicalmechanismofperitonealcarcinomatosisisanindividualsequenceconsistingofgeneticandenvironmentalfactorsandremainscontroversial.Thenaturalhistoryofthediseaserevealsapoormedianprognosisofapproximately6mo;howeveraggressivesurgeryandmultimodaltreatmentoptionscanimproveoncologicoutcomes.Consideringperitonealcarcinomatosisasthoughitisalocoregionaldiseasebutnotametastaticprocess,cytoreductivesurgeryandandintraperitonealchemotherapyhasbeenacurativeoptionduringrecentyears.Cytoreductivesurgeryimpliesaseriesofvisceralresectionsandperitonectomyprocedures.Althoughtheaimofcytoreductivesurgeryistoeliminateallmacroscopicdisease,viabletumorcellsmayremainintheperitonealcavity.Atthatpoint,intraperitonealchemotherapycanextendthemacroscopicdiseaseeliminationtomicroscopicdiseaseelimination.Thesuccessfultreatmentofperitonealcarcinomatosisrequiresacomprehensivemanagementplanincludingproperpatientselection,completeresectionofallvisibledisease,perioperativeintraperitonealchemotherapyandpostoperativesystemicchemotherapy.Surgicalandoncologicoutcomesarestrictlyassociatedwithextentofthetumor,completenessofcytoreductionandpatientrelatedfactorsaswellasmultidisciplinarymanagementandexperienceofthesurgicalteam.Inthisreview,pathophysiologyandcurrentmanagementofperitonealcarcinomatosisoriginatingfromgastrointestinaltumorsarediscussedaccordingtothelatestliterature.

简介：Medicaltherapyfortype2diabetesmellitusisineffectiveinthelongtermduetotheprogressivenatureofthedisease,whichrequiresincreasingmedicationdosesandpolypharmacy.Conversely,bariatricsurgeryhasemergedasacost-effectivestrategyforobesediabeticindividuals;ithaslowcomplicationratesandresultsindurableweightloss,glycemiccontrolandimprovementsinthequalityoflife,obesity-relatedco-morbidityandoverallsurvival.Thefindingthatglucosehomeostasiscanbeachievedwithaweightloss-independentmechanismimmediatelyafterbariatricsurgery,especiallygastricbypass,hasledtotheparadigmofmetabolicsurgery.However,theprimaryfocusofmetabolicsurgeryisthealterationofthephysio-anatomyofthegastrointestinaltracttoachieveglycemiccontrol,metaboliccontrolandcardio-metabolicriskreduction.Todate,metabolicsurgeryisstillnotwelldefined,asitisusedmostfrequentlyforlessobesepatientswithpoorlycontrolleddiabetes.Themechanismofglycemiccontrolisstillincompletelyunderstood.Publishedresearchfindingsonmetabolicsurgeryarepromising,butmanyaspectsstillneedtobedefined.Thispaperexaminestheproposedmechanismofdiabetesremission,theefficacyofdifferenttypesofmetabolicprocedures,thedurabilityofglucosecontrol,andtherisksandcomplicationsassociatedwiththisprocedure.Weproposeatailoredapproachfortheselectionoftheidealmetabolicprocedurefordifferentgroupsofpatients,consideringtheindicationsandprognosticfactorsfordiabetesremission.

简介：CoptotermescurvignathusHolmgren能够在生活树上喂。这个能力被归因于他们由白蚁他们的内脏微生物生产的自己的可加水分解纤维素的酶和合作的酶是有家具的有效消化系统。在这研究，居住在C的内脏的一连串的多样的微生物的身份。curvignathus被定序在全身附近的16SrRNA基因揭示。154细菌的phylotypes的一个总数被发现。Bacteroidetes是最丰富的门并且占了大约65%勇气微生物引起的侧面。这被Firmicutes，Actinobacteria，螺旋菌，Proteobacteria，TM7，Deferribacteres，Planctomycetes，Verrucomicrobia，和白蚁组跟随1。基于种系发生的学习，这共生能是有系统发生的分发，在内脏的强壮的选择压力，和决定细菌的生物群系列在后面的另外的思索的压力的内脏enterotypes的长coevolution的结果。在与另外的白蚁更加不同的细菌的领域的克隆的rRNA基因的种系发生的分发在在哪儿的内脏反映强壮的选择压力C的内脏microbiome的一篇比例的作文。curvignathus建立了。选择压力能被连接到C的唯一的食谱偏爱。深刻地在生活树上喂的curvignathus。精细的内脏microbiome作文可以对机会主义的病原体提供可得到的营养素给主人以及潜在的保护。

简介：AIM:Todeterminethealterationsinratenterocytemitochondrialrespiratoryfunctionandenzymeactivitiesfollowingtraumaticbraininjury(TBI).METHODS:Fifty-sixmaleSDratswererandomlydividedintosevengroups(8ratsineachgroup):acontrolgroup(ratswithshamoperation)andtraumaticbraininjurygroupsat6,12,24h,days2,3,and7afteroperation.TBImodelswereinducedbyFeendy’sfree-fallingmethod.Mitochondrialrespiratoryfunction(respiratorycontrolratioandADP/Oratio)wasmeasuredwithaClarkoxygenelectrode.TheactivitiesofrespiratorychaincomplexⅠ-Ⅳandrelatedenzymesweredeterminedbyspectrophotometry.RESULTS:Comparedwiththecontrolgroup,themitochondrialrespiratorycontrolratio(RCR)declinedat6handremainedatalowleveluntilday7afterTBI(control,5.42±0.46;6h,5.20±0.18;12h,4.55±0.35;24h,3.75±0.22;2d,4.12±0.53;3d,3.45±0.41;7d,5.23±0.24,P<0.01).Thevalueofphosphate-to-oxygen(P/O)significantlydecreasedat12,24h,day2andday3,respectively(12h,3.30±0.10;24h,2.61±0.21;2d,2.95±0.18;3d,2.76±0.09,P<0.01)comparedwiththecontrolgroup(3.46±0.12).Twotroughsofmitochondrialrespiratoryfunctionwereseenat24handday3afterTBI.TheactivitiesofmitochondrialcomplexⅠ(6h:110±10,12h:115±12,24h:85±9,day2:80±15,day3:65±16,P<0.01)andcomplexⅡ(6h:105±8,12h:110±92,24h:80±10,day2:76±8,day3:68±12,P<0.01)wereincreasedat6hand12hfollowingTBI,andthensignificantlydecreasedat24h,day2andday3,respectively.However,therewerenodifferencesincomplexⅠandⅡactivitiesbetweenthecontrolandTBIgroups.Furthermore,pyruvatedehydrogenase(PDH)activitywassignificantlydecreasedat6handcontinuedupto7dafterTBIcomparedwiththecontrolgroup(6h:90±8,12h:85±10,24h:65±12,day2:60±9,day3:55±6,day7:88±11,P<0.01).Thechangesinα-ketoglutaricdehydrogenase(KGDH)activityweresimilartoPDH,exceptthatthedecreaseinKGDHactivitybeganat12hafterTBI(12h:90±12,24h:80±9,day2:76±15,day3:68±7,