简介：Anti-androgentherapyistheleadingtreatmentforadvancedprostatecancerandiscommonlyusedforneoadjuvantoradjuvanttreatment.Bicalutamideisanon-steroidalanti-androgen,usedduringtheinitiationofandrogendeprivationtherapyalongwithaluteinizinghormone-releasinghormoneagonisttoreducethesymptomsoftumor-relatedflaresinpatientswithadvancedprostatecancer.Assideeffects,bicalutamidecancausefatigue,gynecomastia,anddecreasedlibidothroughcompetitiveandrogenreceptorblockade.Additionally,althoughnotascommon,drug-inducedliverinjuryhasalsobeenreported.Herein,wereportacaseofhepatotoxicitysecondarytobicalutamideuse.Typically,bicalutamideinducedhepatotoxicitydevelopsafterafewdays;however,inthiscase,hepaticinjuryoccurred5moaftertreatmentinitiation.Basedonthisrarecaseofdelayedliverinjury,werecommendcarefulmonitoringofliverfunctionthroughoutbicalutamidetreatmentforprostatecancer.

简介：AIM:Toinvestigatetheeffectandmechanismofstimulationofthehypothalamicparaventricularnucleuswithglutamateacidinratswithulcerativecolitis(UC).METHODS:Theratswereanesthetizedwith10%chloralhydrateviaabdominalinjectionandtreatedwithanequalvolumeofTNBS+50%ethanolenema,injectedintotheuppersectionoftheanuswiththetailfacingup.Colonicdamagescoreswerecalculatedafterinjectingacertaindoseofglutamicacidintotheparaventricularnucleus(pVN),andtheeffectofthenucleustractussolitarius(NTS)andvagusnerveinalleviatingUCinjurythroughchemicalstimulationofthepVNwasobservedinrats.ExpressionchangesofC-myc,Apaf-1,caspase-3,interleukin(IL)-6,andIL-17duringtheprotectionagainstUCinjurythroughchemicalstimulationofthepVNinratsweredetectedbyWesternblot.Malondialdehyde(MDA)contentandsuperoxidedismutase(SOD)activityincolontissuesofratsweremeasuredbycolorimetricmethods.RESULTS:ChemicalstimulationofthePVNsignificantlyreducedUCinratsinadose-dependentmanner.TheprotectiveeffectsofthechemicalstimulationofthepVNonratswithUCwereeliminatedafterchemicaldamagetothepVN.AfterglutamatereceptorantagonistkynurenicacidwasinjectedintothepVN,theprotectiveeffectsofthechemicalstimulationofthepVNwereeliminatedinratswithUC.AfterAVpVlreceptorantagonist([Deamino-penl,val4,D-Arg8]-vasopressin)wasinjectedintoNTSorbilateralchemicaldamagetoNTS,theprotectiveeffectofthechemicalstimulationofpVNonUCwasalsoeliminated.AfterchemicalstimulationofthepVN,SODactivityincreased,MDAcontentdecreased,C-mycproteinexpressionsignificantlyincreased,caspase-3andApaf-1proteinexpressionsignificantlydecreased,andIL-6andIL-17expressiondecreasedincolontissuesinratswithUC.CONCLUSION:ChemicalstimulationofthehypothalamicpVNprovidesaprotectiveeffectagainstUCinjuryinrats.HypothalamicpVN,NTSandvagusnerveplayk

简介：InthiseditorialwecommentonthearticlebyFukushiKetalpublishedintherecentissueoftheWorldJournalofGastroenterology2018;24(34):3908-3918.Wefocusspecificallyonthemechanismsoftheanti-thromboticactionofaspirin,gastricmucosalinjuryandaging-relatedincreasedsusceptibilityofgastricmucosatoinjury.Aspiriniswidelyusednotonlyforthemanagementofacuteandchronicpainandarthritis,butalsoimportantlyfortheprimaryandsecondarypreventionofcardiovasculareventssuchasmyocardialinfarctsandstrokes.Clinicaltrialshaveconsistentlyshownthatantiplatelettherapywithlongterm,lowdoseaspirin(LDA)-75to325mgdaily,dramaticallyreducestheriskofnon-fatalmyocardialinfarcts,strokeandmortalityinpatientswithestablishedarterialdiseases.However,suchtreatmentconsiderablyincreasestheriskofgastrointestinal(GI)ulcerationsandseriousbleedingby>2-4fold,especiallyinagingindividuals.ThisriskisfurtherincreasedinpatientsusingLDAtogetherwithotherantiplateletagents,othernonsteroidalanti-inflammatoryagents(NSAIDs)and/oralcohol,orinpatientswithHelicobacterpylori(H.pylori)infection.Previousstudiesbyourgroupandothershavedemonstratedprominentstructuralandfunctionalabnormalitiesingastricmucosaofagingindividuals(whichwerefertoasaginggastricmucosaor“aginggastropathy”)comparedtothegastricmucosaofyoungerindividuals.Aginggastricmucosahasimpairedmucosaldefense,increasedsusceptibilitytoinjurybyavarietyofnoxiousagentssuchasaspirin,otherNSAIDsandethanol,anddelayedandimpairedhealingofinjury.Themechanismunderlyingtheseabnormalitiesofaginggastricmucosaincludereducedmucosalbloodflowcausinghypoxia,upregulationofPTEN,activationofproapoptoticcaspase-3andcaspase-9,andreducedsurvivin(anti-apoptosisprotein),importin-α(nucleartransportprotein),vascularendothelialgrowthfactor,andnervegrowthfactor.Thedecisionregardinginitiationofalong-termLDAtherapyshould

简介：AIM:Tostudytheblockingeffectsofgenisteinoncellproliferationcycleinhumangastriccarcinomacells(SGC-7901)andthepossiblemechanism.METHODS:MTTassaywasappliedinthedetectionoftheinhibitoryeffectsofgenisteinoncellproliferation.Flowcytometrywasusedtoanalyzethecellcycledistribution.ImmunocytochemicaltechniqueandWesternblottingwereperformedtodetecttheproteinexpressionofcyclinD1,cyclinB1andp21waf1/cip1.RESULTS:Genisteinsignificantlyinhibitedthegrowthandproliferationofhumangastriccarcinomacells(SGC-7901).Sevendaysaftertreatmentwithdifferentconcentrationsofgenistein(2.5,5.0,10.0,20.0μg/mL),thegrowthinhibitoryrateswere11.2%,28.8%,55.3%,84.7%respectivelyandcellcycleswerearrestedattheG(2)/Mphase.GenisteindecreasedcyclinD1proteinexpressionandenhancedcyclinB1andp21waf/cip1proteinexpressioninaconcentration-dependentmanner.CONCLUSION:ThegrowthandproliferationofSGC-7901cellscanbeinhibitedbygenisteinviablockingthecellcycle,withreducedexpressionofcyclinD1andenhancedexpressionofcyclinB1andp21waf/cip1proteinintheconcentrationrangeof0-20μg/mL.

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,

简介：背景：训练的整个身体颤动(WBV)出现到豆子为在更老的个人训练的常规抵抗的有效选择。到目前为止，没有数据在心和肺的健康上关于振动效果存在。目的：这随机的ised控制了估计的试用在超过60岁的社区住所成年人在心和肺的健康和肌肉力量上训练的1年的WBV的效果。方法：220个成年人的一个总数(意味着年龄67.1年)随机被分到一个WBV组，健康组或控制组。在一个颤动平台上行使的TheWBV组，和健康组表演了心血管，抵抗，平衡和拉长的锻练。控制组没参予任何训练。心率在一个单个WBV会议期间被测量。山峰氧举起(VO2peak)和time-to-peak锻练(TPE)在进步自行车ergometry期间被测量。肌肉力量被一个测力计估计。结果：心率在WBV训练期间显著地增加了。在1年以后，VO2peak,TPE和肌肉力量在WBV和健康组显著地增加了。两个都训练的组在VO2peak和肌肉力量同样改善了。健康组比WBV组在TPE更显著地改善了。结论：WBV在社区住所训练老看起来有效改进心和肺的健康和肌肉力量。

简介：瞄准：为了在ischemia-reperfusion(红外)上调查rosuvastatin的保护的效果，并且在内皮的氮的氧化物synthase(eNOS)的表示上决定这个代理人的效果，在老鼠导致了小肠的损害和发炎蛋白质。方法：肠的损坏被为30min夹钳优异mes伤寒动脉和腹的箱子在男Sprague-Dawley老鼠导致，为60min由灌注列在后面。在生理盐水溶解的Rosuvastatinintraperitoneally被管理在局部缺血前的60min。肠的粘膜损害和发炎的严厉被几个生物化学的标记，以及由组织检查所见评估。eNOS的蛋白质层次被西方的污点决定。结果：当粘膜的索引损坏，管腔内血红素和蛋白质的层次显著地在假冒操作组与那些相比在红外组被增加。然而，这些增加被处理显著地以一种剂量依赖者方式与rosuvastatin禁止。rosuvastatin的保护的效果被组织检查所见也证实。到红外的小肠的暴露导致了thiobarbituric的重要增加描绘的粘膜发炎酸反应的物质，联系织物的myeloperoxidase活动，和老鼠的粘膜内容导致cytokine的嗜中性的chemoattractant-1(CINC-1)和肿瘤坏死factor-alpha(TNF-alpha)。在红外以后的煽动性的参数的这些增加被预告的处理显著地在10mg/kg的剂量与rosuvastatin禁止。而且，CINC-1和TNF-alpha的mRNA表示在红外以后被增加，并且这增加被rosuvastatin也禁止。eNOS的粘膜蛋白质层次在红外期间减少了，但是在与rosuvastatin对待的老鼠被保存。结论：Rosuvastatin禁止老鼠红外导致的肠的损害和发炎，和它的保护与eNOS的保藏被联系蛋白质。

简介：

简介：瞄准：调查白酒剂量的协会，与反常白酒相关的肝损伤指示物喝和肥胖的持续时间，在中国的岛人口的白酒相关的肝损伤的流行。方法：从中国的岛人口的使随机化的多级式的成层的簇采样在基于人口的盒子控制学习被使用。然后，会见，体格检查，实验室评价和ultrasonography被做。结果：每日的白酒吸入>=20g，喝5年和肥胖是的>=的持续时间仔细与白酒相关的肝损伤有关(P<0.05)。机会比率(或)(95%CI)是1.965(1.122-3.442)，3.412(1.789-6.507)并且1.887(1.261-2.824)分别地。在20g日报白酒吸入组织的>=和20g日报白酒吸入组织的<的白酒相关的肝损伤的流行率分别地是37.14%和12.06%。在喝的5年组织的>=和喝的5年组织的<的白酒相关的肝损伤的流行率分别地是34.44%和8.53%。没有重要剂量反应关系在每日的白酒吸入和反常白酒相关的肝损伤指示物之间以及在喝和反常白酒相关的肝损伤指示物的持续时间之间被发现。在在喝组和黄米饭酒喝酒组，的啤酒之间的白酒相关的肝损伤的流行没有有效差量烈性酒喝酒组，多重喝酒组。结论：每日的白酒吸入的风险阀值是喝导致白酒相关的肝损伤的20g和持续时间在中国的岛人口的5年。肥胖导致的肝损伤应该被担心。

简介：瞄准：为了调查白果树biloba的效果，肺损害上的摘录(EGb761)由肠的ischemia/reperfusion(II/R)导致了。方法：II/R损害的老鼠模型被为灌注为180min跟随的60min夹钳优异mes伤寒动脉生产。老鼠随机被分配进假冒，II/R，和EGb+II/R组。在EGb+II/R组，EGb761(100mg/kg每天)在外科以前经由一个胃的试管被给7连续的天。在II/R和假冒的组的老鼠与EGb761的车辆的相等的体积被对待。肺损害被轻显微镜学，wet-to-dry肺重量比率(W/D)和肺的渗透索引(PPI)估计。malondialdehyde(MDA)和亚硝酸根/硝酸盐的层次(没有(2)(-)/NO(3)(-))，以及超级氧化物歧化酶(草皮)的活动和myeloperoxidase(军邮局)被检验。西方的污点被用来决定可诱导的氮的氧化物synthase(iNOS)的表示。结果：显著地改进的EGb761意味着动脉压和稀释的肺损害，由组织学的变化的改进和肺的W/D和PPI的重要减少表明了(P<0.05或0.01)。而且，EGb761显著地增加了草皮活动，减少的MDA层次和军邮局活动，并且没压制iNOS表示的下面规定伴随的产生(P<0.05或0.01)。结论：结果显示EGb761在II/R导致的肺损害上有保护的效果，它可能与它的抗氧化剂性质和嗜中性的累积的抑制有关并且导致iNOS没有产生。EGb761似乎是为有与II/R有关的呼吸衰竭的非常有病的病人的一个有效治疗学的代理人。