简介：Hamstringmusclestraininjuryisoneofthemostcommoninjuriesinsportsinvolvingsprintingandkicking.Hamstringmusclestraininjuriesoccuratahighrateandhaveahighre-injuryrate,whichresultsinlossoftrainingandcompetitiontime,whichhasasignificantimpactonthequalityoflifeoftheinjuredathletes.~1Preventingandrehabilitatinghamstringmusclestraininjuryisanimportanttaskforcliniciansandscientistsinsportsmedicine.Understandingthemechanismsunderlyinghamstringinjuryiscriticalfordevelopingappropriatestrategiestopreventandrehabilitatehamstringinjuries.Understandingthegeneral

简介：AbstractMany factors can cause inner ear injury, such as noise exposure, chemicals, viral infection, and radiation. The main pathological manifestations of inner ear injury are local hypoxia-ischemia, micro-trauma, and an increased level of reactive oxygen species and inflammatory mediators. The contribution of the inflammatory response to the mediation of cochlear and vestibular pathologies has received increasing attention in recent years. Aseptic inflammation can devastate audition and balance, which can lead to many typical clinical inner ear diseases. In this review, we will discuss the most pertinent and recent research on inflammatory mechanisms in inner ear injury. We will also discuss the pathophysiology of some common and significant ear diseases, such as sudden sensorineural hearing loss, age-related hearing loss, noise-induced hearing loss, and Meniere’s disease.

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简介：Inpatientswhohavesustainedtraumaticbraininjurywithassociatedextremityfracture,thereisoftenaclinicalperceptionthattherateofnewboneformationaroundthefracturesiteincreases.Anovergrowthofcallusisobservedandectopicossificationevenoccursinthemuscle,butthemechanismremainsunclear.Whetherthisrapidly-formednewboneisfracturecallusoravariantofheterotopicossification,acommoncomplicationoftraumaticbrain

简介：WehavecarefullyreadDr.Yuandhiscolleagues'~1reviewonthemechanismofhamstringmusclestraininjuryinsprinting.Thereisnodoubtthattheyhavedonealotworkinthisfield.Theirviewsarebasedon3piecesofevidence.First,observationsfrominsituanimalmodelssuggestthatmusclestraininjuriesarehighlyassociatedwitheccentriccontractions.Second,themagnitudeofmusclestrain,ratherthantheforce,is

简介：<正>Hamstringstrainsareoneofmostcommonsportsinjuries.Thepurposeofthisliteraturereviewistosummarizestudiesonhamstringstraininjuryrate,mechanism,andriskfactorsinthelastseveraldecadeswithafocusonthepreventionandrehabilitationofthisinjury.Hamstringinjurycommonlyoccursinsportingeventsinwhichhighspeedsprintingandkickingarefrequentlyperformed,suchasAustralianfootball.Englishrugby,Americanfootball,andsoccer.Basicsciencestudieshavedemonstratedthatamusclestraininjuryoccursduetoexcessivestrainineccentriccontractioninsteadofforce,andthatelongationspeedanddurationofactivationbeforeeccentriccontractionaffecttheseverityoftheinjury.Hamstringstraininjuryislikelytooccurduringthelateswingphaseandlatestancephaseofsprintrunning.Shortenedoptimummusclelength,lackofmuscleflexibility,strengthimbalance,insufficientwarm-up,fatigue,lowerbackinjury,poorlumbarposture,andincreasedmuscleneuraltensionhavebeenidentifiedasmodifiableriskfactorswhilemusclecompositions,age,race,andpreviousinjuriesarenon-modifiableriskfactors.Thetheoreticalbasisofsomeoftheseriskfactors,however,islacking,andtheresultsofclinicalstudiesontheseriskfactorsareinconsistent.Futurestudiesareneededtoestablishthecause-and-effectrelationshipsbetweenthoseproposedriskfactorsandtheinjury.

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简介：Objective:Toevaluatetheprotectiveeffectsof8%emulsifiedisofluraneaftermyocardialischemia-reperfusioninjuryanditsmechanisminrabbits.Methods:Twenty-fourmaleadultNewZealandwhiterabbitswereanesthetizedwithintravenousinjectionof30mg/kgpentobarbitalfollowedby5mg·kg-1·h-1infusion.Allrabbitsweresubjectedto30minutesofleftanteriorde-scendingcoronaryartery(LAD)occlusionand3hoursofsubsequentreperfusion.BeforeLADocclusion,therabbitswererandomlyallocatedintothreegroupsforprecondi-tioningtreatment(eightforeachgroup).Thecontrolgroup(Cgroup)receivedintravenously0.9%NaClfor30minutes.Theemulsifiedisofluranegroup(EIgroup)received8%emulsifiedisofluraneintravenouslytill0.64%end-tidalcon-centrationfor30minutesthatwasfollowedbya15-minutewashoutperiod.TheIntralipidgroup(INgroup)received30%Intralipidfor30minutes.Theinfarctedarea,plasmamalondialdehyde(MDA)content,superoxidedismutaseactivity(SOD)andnitriteconcentrationafter3-hourmyo-cardialperfusionwererecordedsimultaneously.Results:Forthemyocardialischemia-reperfusionin-juryanimals,theinfarctedsizeintheEIgroupwassignifi-cantlyreduced(91.9%±8%)ascomparedwithcontrolgroup(39%±6%,t=5.19,P<0.01).TheplasmaSODactivityandnitriteconcentrationinEIgroupweresignificantlyhigherthanthoseincontrolgroup(t=2.82,t=8.46,P<0.05),butMDAcontentwaslowerinEIgroupthanthatincontrolgroup(t=2.56,P<0.05).Conclusions:Theresultsindicatethatemulsifiedisofluranehasacardioprotectioneffectagainstischemia-reperfusioninjury.ThisbeneficialeffectofemulsifiedisofluraneisprobablythroughNOreleaseandconsequentlybyincreaseinautioxidationofmyocardium.

简介：AbstractCoronavirus disease 2019 is a major threat to public health globally. Though its pathogenesis has not been fully elucidated, angiotensin-converting enzyme 2 (ACE2) has been recently identified as a receptor for the entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into the cell. Here, we aimed to clarify the potential role of ACE2 in SARS-CoV-2-induced acute lung injury and its underlying mechanism. As a receptor for coronavirus, ACE2 mediates the entry of SARS-CoV-2 into cells in a similar way as for severe acute respiratory syndrome coronavirus (SARS-CoV). The high binding affinity of SARS-CoV-2 to ACE2 correlates with its efficient spread among humans. On the other hand, ACE2 negatively regulates the renin-angiotensin-aldosterone system (RAAS) primarily by converting angiotensin II to angiotensin 1-7, which exerts a beneficial effect on coronavirus-induced acute lung injury. Human recombinant ACE2 has been considered as a potential therapy for SARS-CoV-2 by blocking virus entry and redressing the imbalance of RAAS in SARS-CoV-2 infection. The level of ACE2 expression can be upregulated by treatment with an ACE inhibitor (ACEI) or angiotensin II type 1 receptor blocker (ARB). To date, no evidence shows that ACEIs or ARBs increase the susceptibility and mortality of patients infected with SARS-CoV-2, and hence, it is not advisable to discontinue such drugs in patients with cardiovascular disease.

简介：Vagusnervestimulationexertsprotectiveeffectsagainstischemicbraininjury;however,theunderlyingmechanismsremainunclear.Inthisstudy,aratmodeloffocalcerebralischemiawasestablishedusingtheocclusionmethod,andtherightvagusnervewasgivenelectricalstimulation(constantcurrentof0.5mA;pulsewidth,0.5ms;frequency,20Hz;duration,30seconds;every5minutesforatotalof60minutes)30minutes,12hours,and1,2,3,7and14daysaftersurgery.Electricalstimulationofthevagusnervesubstantiallyreducedinfarctvolume,improvedneurologicalfunction,anddecreasedtheexpressionlevelsoftumornecrosisfactor-αandinterleukin-6inratswithfocalcerebralischemia.Theexperimentalfindingsindicatethattheneuroprotectiveeffectofvagusnervestimulationfollowingcerebralischemiamaybeassociatedwiththeinhibitionoftumornecrosisfactor-αandinterleukin-6expression.

简介：Menofreproductiveageundergoingradiotherapyareoftenconcernedaboutthepossibleeffectsonfertilityandfuturechildren[1].Inthisinvestigation,serumtestosteronewasmeasuredfollowingwhole-bodyirradiationwitha2Gycarbonionradiation(CIR),andimmunofluorescencewereusedtoinvestigateproteinlocalizationthatevaluatetheunderlyingtoxicologicalmechanismofacuteinjuryinducedbyCIRinpubertalmicetestes.

简介：Theincreaseinneurotrophicfactorsaftercraniocerebralinjuryhasbeenshowntopromotefracturehealing.Moreover,neurotrophicfactorsplayakeyroleintheregenerationandrepairofperipheralnerve.However,whethercraniocerebralinjuryalterstherepairofperipheralnerveinjuriesremainspoorlyunderstood.Ratinjurymodelswereestablishedbytransectingtheleftsciaticnerveandusingafree-falldevicetoinducecraniocerebralinjury.Comparedwithsciaticnerveinjuryaloneafter6–12weeks,ratswithcombinedsciaticandcraniocerebralinjuriesshoweddecreasedsciaticfunctionalindex,increasedrecoveryofgastrocnemiusmusclewetweight,recoveryofsciaticnervegangliaandcorrespondingspinalcordsegmentneuronmorphologies,andincreasednumbersofhorseradishperoxidase-labeledcells.Theseresultsindicatethatcraniocerebralinjurypromotestherepairofperipheralnerveinjury.

简介：客观：为了改进痊愈，与由craniocerebral损害复杂的腹的内脏的损害病人评价。方法：由craniocerebral损害复杂的腹的内脏的损害的176个盒子的临床的数据回顾地被分析。结果：在这个系列，44个盒子死了，死亡是25.0%。死亡的主要原因是与吃惊相结合的腹的内脏的损害和严重craniocerebral损害。结论：在早舞台由精确诊断改进痊愈率是必要的。腹的帕拉穿刺术和CT应该即时并且动态地被执行。优先级应该被给life-threateninginjuries的治疗。

简介：Thephenomenonofischemia/reperfusioninjuryisdescribedintheexperimentalmodelsofacutemyocardialinfarction(AMI),causingadditionalfunctionalandstructuraldamagetotheacutereperfusedmyocardium,andischemicpreconditioningreferstothemyocardialischemiaafteralongperiodofreperfusionbeforeoneorseveralshortoccasionalduplicationofmyocardialischemia/reperfusion1,whichcanincreasemyocardialischemictolerance.ThetherapeuticstrategiesforAMIhavefocusedonmyocardialischemia/reperfusioninjury,whichaccountsforasignificantpartofthefinalinfarctsize.Althoughexperimentsinthelast20yearshavereportedthatpharmacologicalinterventionsatreperfusionmightreducemyocardialreperfusioninjury,thiscouldnotbeconfirmedinhumanstudies.Analternativetochemicalmodifiers,postconditioning(briefrepeatedperiodsofischemiaappliedattheonsetofreperfusion)isanothermethodproventobeefficientinanimalmodelsandtobeconfirmedinrecenthumanstudies.Thissimplemethod,appliedinthefirstminuteofreperfusion,reducesthefinalinfarctsizeby30%-50%.Thisreviewwillfocusonthemechanisms,pharmacologicalpreconditioning,postconditioningtechnique,whichiseasilyapplicableinhumanpatientsinthesettingofAMI.

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简介：Thecingulum,theneuraltractconnectingtheorbitofrontalcortexwiththemedialtemporallobe,playsanimportantroleincognition(Bushetal.,2000).Itisalsoimportantinmemorybecauseitprovidescholinergicinnervationstothecerebralcortexafterobtaininginnervationfromthemedialseptalnucleus,the

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简介：Theadipocytokine,apelin-13,isanabundantlyexpressedpeptideinthenervoussystem.Apelin-13protectsthebrainagainstischemia/reperfusioninjuryandattenuatestraumaticbraininjurybysuppressingautophagy.However,secondaryapelin-13effectsontraumaticbraininjury-inducedneuralcelldeathandblood-brainbarrierintegrityarestillnotclear.Here,wefoundthatapelin-13significantlydecreasescerebralwatercontent,mitigatesblood-brainbarrierdestruction,reducesaquaporin-4expression,diminishescaspase-3andBaxexpressioninthecerebralcortexandhippocampus,andreducesapoptosis.Theseresultsshowthatapelin-13attenuatessecondaryinjuryaftertraumaticbraininjuryandexertsaneuroprotectiveeffect.

简介：Inflammationafterstrokeisthemaincauseofcerebralischemia/reperfusioninjury.Cascadingeventsafterinjurycanleadtocelldeath.Heatshockprotein70andotherendogenousinjury-signalingmoleculesarereleasedbydamagedcells,whichcanleadtosystemicstressreactions.Protectingthebrainthroughrepairbeginswiththestress-injury-repairsignalingchain.Thisstudyaimedtoverifywhetheracupunctureactsthroughthischaintofacilitateeffectivetreatmentofischemicstroke.Ratmodelsofcerebralischemia/reperfusioninjurywereestablishedbyZeaLonga'smethod,andinjurysiteswereidentifiedbyassessingneurologicalfunction,2,3,5-triphenyltetrazoliumchloridestaining,andhematoxylin-eosinstaining.ElectroacupunctureatacupointsBaihui(DU20)andZusanli(ST36)wasperformedinthemodelratswithdilatationalwaves,deliveredfor20minutesadayat2–100Hzandanamplitudeof2mA.Weanalyzedthebloodserumfromtheratsandfoundthatinflammatorycytokinesaffectedthelevelsofadrenotrophinandheatshockprotein70,eachofwhichfollowedasimilarbimodalcurve.Specifically,electroacupunctureloweredthepeaklevelsofadrenocorticotrophichormoneandheatshockprotein70.Thus,electroacupuncturewasabletoinhibitexcessivestress,reduceinflammation,andpromotetherepairofneurons,whichfacilitatedhealingofischemicstroke.