简介：Oxidativestressiscloselyassociatedwithsecondarycelldeathinmanydisordersofthecentralnervoussystemincludingstroke,Parkinson’sdisease,Alzheimer’sdisease.Amongmanyaberrantoxidativestress-associatedproteins,DJ-1hasbeenassociatedwiththeoxidativestresscelldeathcascadeprimarilyinParkinson’sdisease.Althoughprincipallyexpressedinthecytoplasmandnucleus,DJ-1canbesecretedintotheserumunderpathologicalcondition.Recently,aclosepathologicalassociationbetweenDJ-1andoxidativestressinstrokehasbeenimplicated.Tothisend,weandothershavedemonstratedtheimportantroleofmitochondriainneuroprotectionforstrokebydemonstratingthatthetranslocationofDJ-1inthemitochondriacouldpotentiallymitigatemitochondrialinjury.Here,wediscussourrecentfindingstestingthehypothesisthatDJ-1notonlyfunctionsasaformofintracellularprotectionfromoxidativestress,butthatitalsoutilizesparacrineand/orautocrinecuesinordertoaccomplishextracellularsignalingbetweenneighboringneuronalcells,resultinginneuroprotection.ThisarticlehighlightsrecentevidencesupportingthestatusofDJ-1askeyanti-oxidativestresstherapeutictargetforstroke.

简介：“一步一步走过昨天我的孩子气。我的孩子气给我勇气。”依然在听着《after17》，Cheer的声音有种超脱了年龄的纯粹，我想起新东方课上思思说起他英文名时无比骄傲的样子：FS——ForeverSeventeen。我已经离17岁很远很远了，远到我甚至开始模糊了那一段黑暗而青涩的记忆。

简介：Idon'tthinkIevenopenedmyeyeswhenDerekkissedmegood-byethatmorning.Yourememberthingslikethatafterward.Fivemonthspregnantwithoursecondchildandwornoutfromrunningafter13-month-oldTyler,IgrabbedeverymomentofsleepIcould.

简介：这研究的目的是在老鼠模型在肝移植以后在早时期(24h)观察在接枝的损害和氧化还原作用factor-1(Ref-1)的表示之间的关系。150只成年男威斯特老鼠随机包括肝被划分成三个组移植组，假冒的外科组和未经治疗的控制组。在肝移植以后，动物在不同时间点被牺牲，并且Ref-1的表示的变化和意义然后被immunohistochemistry，血清学和组织病理学说探索。作为与假冒的外科组和未经治疗的控制组相比，Ref-1蛋白质在的表示移植组在在肝移植以后的早时期是更强壮的。与病理分析，大量渗透的发炎房间在门静脉附近被发现。肝的纸巾是损害。然而，在假冒的外科的损害和未经治疗的控制组是比较地细微的。浆液中高音和著名计算机生产厂商层次在6-12h到达了山峰，并且在12h以后显著地减少了。这些数据建议在在移植以后的更早的时期的肝损害的度在6h达到顶点然后减少。并且Ref-1蛋白质由肝的ischemic灌注损害导致了可能在修理损害起一个关键作用。

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简介：BackgroundCoronarymicroembolization(CME)ischaracterizedbydistalmicrovascularocclusion.However,theinflammatorymechanismsandtherapeutictargetsofCMEarelargelyunknown.MethodsAtotalof11GuangxiBamaminiatureswinesweredividedintotwogroups:sham(n=5)andCME(n=6).MicrosphereswereinjectedintotheleftanteriordescendingarteryoftheCMEgrouptomakeananimalmodelofCME.TheexpressionsofmicroRNA-146a(miR-146a)andIRAK1,TRAF6,andAUF1inthemyocardiumweredetectedbyqPCR.ResultsIntheCMEgroup,microspheres,microinfarction,andinflammatorycellinfiltrationwerefoundunderanopticalmicroscope.TheexpressionlevelsofmiR-146awerelowinbothgroups.AfterCME,theexpressionlevelsofIRAK1,TRAF6,andAUF1intheCMEgroupwereupregulatedcomparedwiththoseintheshamgroup(P<0.01;P<0.05;P<0.05,respectively).ConclusionsAUF1,IRAK1andTRAF6,butnotmiR-146a,couldbeinvolved,inmyocardiuminflammationfollowingCME.

简介：AbstractBackground:Macrophages play an important role in renal ischemia reperfusion injury, but the functional changes of macrophages under hypoxia/reoxygenation and the related mechanism are unclear and need to be further clarified.Methods:The effects of hypoxia/reoxygenation on functional characteristics of RAW264.7 macrophages were analyzed through the protein expression detection of pro-inflammatory factors TNF-α and CD80, anti-inflammatory factors ARG-1 and CD206. The functional implications of C-X3-C motif chemokine receptor 1(CX3CR1) down-regulation in hypoxic macrophages were explored using small interfering RNA technology. Significance was assessed by the parametric t-test or nonparametric Mann-Whitney test for two group comparisons, and a one-way ANOVA or the Kruskal-Wallis test for multiple group comparisons.Results:Hypoxia/reoxygenation significantly increased the protein expression of M1-related pro-inflammatory factors TNF-α, CD80 and chemokine C-X3-C motif chemokine ligand 1 (CX3CL1)/CX3CR1 and inhibited the protein expression of M2-related anti-inflammatory factors ARG-1 and CD206 in a time-dependent manner in RAW264.7 cells. However, the silencing of CX3CR1 in RAW264.7 cells using specific CX3CR1-siRNA, significantly attenuated the increase in protein expression of TNF-α (P < 0.05) and CD80 (P < 0.01) and the inhibition of ARG-1 (P < 0.01) and CD206 (P < 0.01) induced by hypoxia/reoxygenation. In addition, we also found that hypoxia/reoxygenation could significantly enhance the migration (2.2-fold, P < 0.01) and adhesion capacity (1.5-fold, P < 0.01) of RAW264.7 macrophages compared with the control group, and CX3CR1-siRNA had an inhibitory role (40% and 20% reduction, respectively). For elucidating the mechanism, we showed that the phosphorylation levels of ERK (P < 0.01) and the p65 subunit of NF-κB (P < 0.01) of the RAW264.7 cells in the hypoxic/reoxygenation group were significantly increased, which could be attenuated by down-regulation of CX3CR1 expression (P < 0.01, both). ERK inhibitors also significantly blocked the effects of hypoxic/reoxygenation on the protein expression of M1-related pro-inflammatory factors TNF-α, CD80 and M2-related anti-inflammatory factors ARG-1 and CD206. Moreover, we found that conditioned medium from polarized M1 macrophages induced by hypoxia/reoxygenation, notably increased the degree of apoptosis of hypoxia/reoxygenation-induced TCMK-1 cells, and promoted the protein expression of pro-apoptotic proteins bax (P < 0.01) and cleaved-caspase 3 (P < 0.01) and inhibited the expression of anti-apoptotic protein bcl-2 (P < 0.01), but silencing CX3CR1 in macrophages had a protective role. Finally, we also found that the secretion of soluble CX3CL1 in RAW264.7 macrophages under hypoxia/reoxygenation was significantly increased.Conclusions:The findings suggest that hypoxia/reoxygenation could promote M1 polarization, cell migration, and adhesion of macrophages, and that polarized macrophages induce further apoptosis of hypoxic renal tubular epithelial cells by regulating of CX3CL1/CX3CR1 signaling pathway.

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简介：在拯救了PrincessFiona（菲奥娜公主），寻找到了真爱。并做了三个孩子的父亲之后，我们的Shrek（史莱克）成了一个居家好男人。但是，家庭生活是繁杂的，随着时间的飞逝，Shrek开始怀念过去。向往重新做回怪物，过自由自在、无拘无束的生活。

简介：放学后,你通常会干什么？和同学玩耍？还是回家做作业？想知道美国的小学生放学后都会做什么吗？

简介：ObjectivesToinvestigatetheeffectsofadrenergicreceptorantagonist(metoprololorprazosin)onmyocardialα1-ARdensityandthechangesofventriculareffectiverefractoryperioddispersion(VERP-D)inrabbitsaftermyocardialinfarction.Methodstwenty-fouradultmaleNewZealandrabbitsweredividedintofourgroupsatrandom:controlgroup(n=6);MIwithplacebogroup(n=6);MIwithmetoprololgroup(n=6);MIwithprazosingroup(n=6).Therabbitsreceivedcorrespondingdrugsforsevendays,beginningatthefirstdayafterMIandmyocardialα1-ARdensityweremeasuredandmeanwhile,myocardialβ-ARwasalsomeasured.ResultsIntheplacebogroup,thedensityofventricularα1-ARwasincreasedincomparisonwithcontrolgroup(α1-ARinnormalregion36.9±0.2vs27.3±0.9fmolmg-1Pro-1,p＜0.01;α1-ARinischemicregion33.0±0.9vs26.6±0.4fmolmg-1pro-1P＜0.01).Inthemetoprololgroup,itwasalsoincreasedincomparisonwithcontrolgroup(α1-ARinnormalregion44.7±1.5vs27.3±0.9fmolmg-1pro-1,P＜0.01;α1-ARinischemicregion33.6±0.5vs26.6±0.4fmolmg-1pro-1,P＜0.01).Meanwhilethedensityofventricularα1-ARinnormalregioninthemetoprololgroupwasincreasedincomparisonwithplacebogroup(44.7±1.5vs36.9±0.2fmolmg-1pro-1,P＜0.01).Whileitdecreasedintheprazosingroupincomparisonwithcontrolgroup(α1-ARinnormalregion22.5±0.6vs27.3±0.9fmolmg-1pro-1,P＜0.01;α1-ARinischemicregion20.9±0.4vs26.6±0.4fmolmg-1pro-1,P＜0.01).VERP-DwasincreasedafterMI(P＜0.01).Aftertreatmentwithmetoprololorprazosin,VERP-Dwasdecreased(P＜0.01).ConclusionsAfteracuteMI,α1-ARofventricularmyocardiumwasupregulated,whichmaybeaccompaniedbyitsactivitation.Thedensityofmyocardialα1-ARbecameupregulatedmoredramaticallytreatedwithmetoprololanddownregulatedwithprazosin.Whentreatedwithmetoprololorprazosin,VERP-Ddecreased.

简介：Objective:ToobservetheeffectsofgangliosideGM1onreductionofbrainedemaandameliorationofcerebralmetabolismaftertraumaticbraininjury(TBI).Methods:AnacuteexperimentalclosedTBImodelinratswasinducedbyafluid-percussionbraininjurymodel.AtfiveandsixtyminutesafterTBI,theanimalswereintraperitoneallyinjectedbygangliosideGM1(30mg/kg)orthesamevolumeofsaline.Atthe6thhourafterTBI,effectsofgangliosideGM1orsalineonchangesofmeanarterialpressure(MAP),contentsofwater,lacticacid(LA)andlipipperoxidation(LPO)intheinjuredcerebraltissueswereobserved.Results:AfterTBI,MAPdecreasedandcontentsofwater,LAandLPOincreasedinbraininjurygroup;however,MAPwasbacktonormallevelsandcontentsofwater,LAandLPOdecreasedingangliosideGM1treatedgroup,comparedwiththoseinbraininjurygroup(P<0.05).Nosignificantdifferencebetweenthesalinetreatedgroupandthebraininjurygroup(P>0.05)wasobserved.Conclusions:GangliosideGM1doeshaveobviousneuroprotectiveeffectonearlyTBI.

简介：InordertoexploretheabnormalvariationsbeforeandaftertheWen'anM5.1earthquakeonJuly4,2006,thegravitydataobservedbytheWenbaGravityObservationNetworkbeforeandaftertheearthquakewasanalyzed.Therelationshipsbetweengravitychangeandverticaldisplacementandshallowgroundwaterlevelwerediscussed,andelevationcorrectionofthegravitywaspreliminarilyperformed.TheresultsshowthattherewereabnormalgravitychangesbeforetheM5.1earthquake,whichappearedasgravityrisinginthewholeobservationnetwork,especiallyinthesouthpart.AhighgradientofgravityvariationappearedaroundtheepicenterbeforetheM5.1earthquake,especiallyduringtheshortperiodbetweenOctober2005toApril2006.TheboundaryofthepositiveandnegativegravityvariationsgraduallydeflectedandbegantorecoverfromOctober2007.

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简介：BACKGROUND:Epidemiologicstudieshaveindicatedthattheincidenceofstrokeinpremenopausalfemalesislowerthaninmalesatthesameage,butitsignificantlyrisesinpostmenopausalfemales.Estrogenisusedclinicallytoalleviateinjurycausedbycerebralischemia.Ithasbeenhypothesizedthattheneuroprotectiveroleofestrogenrelatestoangiopoietin(Angpt),whichplaysanimportantroleinvascularization,vascularremodelingandmaturation.OBJECTIVE:Toobserveandvalidatetheeffectofestradiolonangiopoietin-1(Angpt1)mRNAexpressioninovariectomizedratswithfocalcerebralischemiaafterreperfusion,soastoexplorethemolecularmechanismsofestradiol-mediatedprotectionfromcerebralischemicdamage.DESIGN,TIMEANDSETTING:Randomized,controlled,molecularbiology,prospectiveanimalstudy.TheexperimentwasperformedattheCentralLaboratoryofChongqingMedicalUniversityfromSeptembertoDecember2005.MATERIALS:Fiftyhealthyfemalewildtype(WT)ratsaged6monthsandfiftyfemaleratsaged6monthswithknockoutoftheestrogen-alphareceptorgene(ERKO).METHODS:WTratsandERKOratsweredividedintoestradiolandcontrolgroups(n=25),andinjectedin-tramuscularlywithestradiolbenzoate(100μg/kgperday)orcornoil(1mL/kgperday)for7days,30daysafterbilateralovariectomy.Ratmodelsofcerebralischemia/reperfusionwereestablishedwiththemiddlecerebralarteryocclusionmethod.After30minutesofmiddlecerebralarteryocclusion,ratsfromtheestradiolandcontrolgroupswereinjectedintramuscularlywithestradiolbenzoateorcornoilattheabovedose.MAINOUTCOMEMEASURES:Weusedradio-immunityanalysisandlaser-Dopplerflowmetrytomeasureplasmaestradiollevelsandchangesincerebralbloodflow.WeusedimmunohistochemicalstainingofCD34epitopestomeasurechangesinthecapillarydensityinbrainfollowingcerebralischemia/reperfusion,andquantitativeRT-PCRanalysistoassessmRNAexpressionlevelsofAngpt1,Angpt2,Tie2,vascu

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简介：Intherecentpresidentialelection,amostbittertrialofstrengthsinceitsinde-pendencetookplacebetweenthe“democrats”andtheso-called“traditionalists”inRussia.TheoutcomeofthisrivalryhasadirectbearingonthechoiceofRussia’sfuturedevelopmentpath.ThereelectionoftheincumbentPresi-dentBorisYeltsininthesecondroundofthevotinghasofferedthepoliticalguaran-teeforthecountry’sfurthersearchforanappropriatedevelopmentstrategyalongthecurrenttrack.

简介：AbstractBackground:Despite advances in decompressive craniectomy (DC) for the treatment of traumatic brain injury (TBI), these patients are at risk of having a poor long-term prognosis. The aim of this study was to predict 1-year mortality in TBI patients undergoing DC using logistic regression and random tree models.Methods:This was a retrospective analysis of TBI patients undergoing DC from January 1, 2015, to April 25, 2019. Patient demographic characteristics, biochemical tests, and intraoperative factors were collected. One-year mortality prognostic models were developed using multivariate logistic regression and random tree algorithms. The overall accuracy, sensitivity, specificity, and area under the receiver operating characteristic curves (AUCs) were used to evaluate model performance.Results:Of the 230 patients, 70 (30.4%) died within 1 year. Older age (OR, 1.066; 95% CI, 1.045-1.087; P < 0.001), higher Glasgow Coma Score (GCS) (OR, 0.737; 95% CI, 0.660-0.824; P < 0.001), higher D-dimer (OR, 1.005; 95% CI, 1.001-1.009; P = 0.015), coagulopathy (OR, 2.965; 95% CI, 1.808-4.864; P < 0.001), hypotension (OR, 3.862; 95% CI, 2.176-6.855; P < 0.001), and completely effaced basal cisterns (OR, 3.766; 95% CI, 2.255-6.290; P < 0.001) were independent predictors of 1-year mortality. Random forest demonstrated better performance for 1-year mortality prediction, which achieved an overall accuracy of 0.810, sensitivity of 0.833, specificity of 0.800, and AUC of 0.830 on the testing data compared to the logistic regression model.Conclusions:The random forest model showed relatively good predictive performance for 1-year mortality in TBI patients undergoing DC. Further external tests are required to verify our prognostic model.